What if the conventional wisdom on fixing broken
bones isn't quite right? Imagine looking at a
classic medical text over 70 years old that suggests
sometimes less is actually more. Right. That
trying too hard to achieve perfect anatomical
alignment can, counterintuitively, lead to a
worse outcome. That's a fascinating idea. Welcome
back to The Deep Dive, the show where we take
a stack of sources, whether they're complex reports,
foundational texts, or groundbreaking research,
and extract the most important nuggets of knowledge
for you. Our mission is always to give you that
shortcut to being well -informed with surprising
facts and enough context to make it stick. Absolutely.
Today we're embarking on a deep dive into a fascinating
piece of medical history that offers enduring
lessons. Excerpts from John Charnley's seminal
1950 text, the closed treatment of common fractures.
A real classic. It is. And this isn't just about
old medical techniques. It's a deep look at fundamental
principles of healing, mechanics, and biological
reality that shaped how surgery evolved and still
resonate today. Definitely. It's about the thinking
behind it. It is, yes. It's about challenging
assumptions and understanding the why. I'm joined,
as always, by our expert speaker, a mind capable
of synthesizing complex information and providing
the essential context needed to navigate these
deep dives. It's a real privilege to explore
this text. Charnley's work is, well, it's a brilliant
example of rigorous observation and critical
thinking applied to clinical problems. It really
is. And its insights, I think, extend far beyond
just the operating theater. Absolutely. reading
this book published right at the midpoint of
the 20th century, you're struck by how much has
changed in surgery, of course, but also how many
of his core arguments feel incredibly relevant,
even provocative today. They do. He was clearly
pushing against the prevailing tides in some
areas, wasn't he? Certainly. He wasn't afraid
to challenge established views. Let's jump straight
into a rapid fire set up then. pulling out a
few high impact points from the book to preview
some of the fascinating angles we'll explore.
Sounds good. First question, drawn from the very
beginning of the book. Charlie dives straight
into the difficulty of scientifically comparing
conservative closed methods of fracture treatment,
things like manipulation and plaster casts, with
operative surgical treatment. Right, the classic
comparison. Exactly. Why was a true comparison
based on hard data so challenging even back then,
and what were some of the surprising downsides
he highlighted about the surgical approaches
prevalent at the time? A crucial starting point
for the book, really. Yeah. And it highlights
the state of medical understanding and, well,
research methodology back then in the mid -20th
century. How so? Charlie is quite clear that
a true rigorous comparison was difficult because,
well, as he puts it, the fundamental nature of
fracture repair was unknown from a basic science
perspective. So they knew things healed. But
not precisely how. Exactly. Healing was observed
clinically, of course, but the underlying cellular,
the molecular processes, they were poorly understood.
So clinical practice was the primary, almost
the only way to compare methods. The clinical
results were plagued by variables. Too many confounding
factors. Precisely. Think about the complexity.
The degree of bone fragmentation was called comminution,
where the bone shatters into multiple pieces.
The presence or absence of infection, sepsis.
The specific surgical technique used, the surgeon's
own skill. Huge variables there. Huge. And the
patient's overall health, the blood supply to
the bone, the location of the fracture itself,
who is assessing the outcome? All these factors
varied enormously. So trying to pool results
was almost impossible. Well, it made pooling
results from even a series of, say, one or two
hundred cases statistically insignificant when
trying to draw firm conclusions about which method
was inherently better. Right. You couldn't isolate
the variables. Not effectively. And on top of
this, he noted significant downsides to the operative
treatments of the era. Early internal fixation
involved implants that were mechanically limited.
And weren't strong enough. He talks about the
enormous that bones are subjected to, you know,
just through normal movement. And the mental
implants of the time were prone to fatigue failure.
Meaning they'd just break. They would break under
repeated stress, often before the healing was
complete. Ah, not ideal. Not ideal at all. And,
critically, there was a significant risk of sepsis
infection associated with surgery. A risk that,
according to Charlie, was greatly exacerbated
by specific surgical steps. Which steps in particular?
Particularly stripping away the periosteum. from
the bone surface, that outer membrane. OK, we'll
definitely come back to the periosteum. So messy
data, early tech with failure points. It paints
a different picture than our modern assumptions
about surgical certainty, doesn't it? It really
does. A much less certain picture. Second rapid
-fire question, then, and this relates to one
of his core arguments. Charnley repeatedly steers
attention away from the broken bone fragments
themselves and towards something else entirely.
What does he suggest is actually more important
than those broken ends in guiding a successful
fracture reduction? This is where Charnley truly
challenges the, well, the visually obvious, which
you see on the x -ray. While x -rays show us
the bone fragments clear as day, he argues that
the supreme importance of the soft tissues is
often forgotten precisely because they are radiotranslucent.
They don't show up well on the x -ray. Exactly.
Yet these soft tissues, the muscles, ligaments,
the joint capsule, the periostome, as mentioned,
he presents them as secondary only to life itself
in the process of healing and critically in guiding
a close reduction. when you're manipulating the
limb without cutting it open. So how do they
guide it? It's the undamaged soft parts you see.
The bits that aren't torn, they act like a hinge
or a guiding tether. They provide the crucial
clue to successful closed reduction. Ah, right.
If you could manipulate the limb to bring these
intact soft tissues back into their normal anatomical
relationship, the bone fragments even if you
can't see them perfectly on an x -ray, will often
just fall back into place. They follow the lead
of the tissues still holding things together.
That concept of the soft tissue hinge of the
invisible guiding the visible, that's incredibly
powerful. It really is a fundamental insight.
OK, final rapid fire point. He also challenges
assumptions about plaster casts and splinting.
What's a key takeaway from the book about how
a plaster actually works or perhaps how it doesn't
work? in providing fixation. Right, the plaster
cast. The common image is one of absolute rigidity,
isn't it? Holding everything perfectly still.
Yes, like concrete. But Charlie explains that
a plaster functions not just as a passive mold,
but through what he calls a three -point system.
Three points. Yes. Imagine applying force at
three specific points, two points on one side
of the limb and a third point on the opposite
side, usually right at the level of the fracture,
pushing against the other two. Okay, I can picture
that. This system exerts counter pressure to
maintain alignment, which is why the molding
of the plaster as it sets is so important. Ah,
it's not just wrapping it on. Not at all. Sometimes
you need a plaster that's actually slightly curved
to hold a straight bone in place because of the
forces it needs to exert. Okay, but you said
how it doesn't work, too. Yes, and this is the
critical point. Even the most meticulously applied
skin -tight plaster only provides relative immobilization.
Relative. Not absolute. Not absolute, no. True,
absolute immobilization, eliminating even microscopic
movement at the fracture site. That's only possible
with internal fixation metal plates or rods inside
the body. Why can't plaster achieve that? The
reason is the movement that occurs between the
skin and the skeleton. The skin moves relative
to the bone underneath, doesn't it? Yes, a little
bit. And the plaster is essentially fixed to
the skin. So any skin movement means some movement
potential at the fracture. He points out that
even with a wrist fracture cast, a patient can
often still manage half an inch or so of wrist
movement. I never thought of it like that. And
he's particularly, well, quite scathing about
walking plasters for foot fractures. Things in
the tarsus or metatarsus. The bones in the midfoot
and towards the toes. Exactly. He basically says
they are no more effective than a leather boot
for immobilizing the bone itself. Really? That's
strong. Yes. Because as you bear weight, the
soft tissues of the soul compress, the foot arches
deflect. There's movement, regardless of the
cast. The cast is just a shell around a structure
that's inherently moving internally under load.
So even something we see as incredibly solid,
like a plaster cast, is presented as only providing
relative fixation due to the very biological
reality of skin and tissue movement. That's his
argument, yes. That genuinely makes you look
at a cast differently. OK. fascinating groundwork
laid. Let's unpack this further and move into
our first major segment, Foundations and Fundamentals,
delving deeper into the underlying biological
and mechanical principles Charnley explores in
the book. Absolutely. The book really starts
by looking at the fundamental nature of bone
healing. A process that, you have to remember,
was still being actively researched and debated
in his time. Right. He touches on the different
types of bone tissue woven bone, which is the
initial, maybe slightly hurried, provisional
bone laid down quickly after injury. Gives early
stability. Like a quick patch job. Sort of, yes.
And then there's lamellar bone, which is the
stronger, more organized layered structure that
forms later. It needs that initial woven scaffold
to mature properly. Think of woven bone as maybe
the temporary scaffolding put up quickly on a
building site, and lamellar bone as the eventual
reinforced concrete structure being carefully
built layer by layer upon it. That's a helpful
analogy. And this is where he introduces his
strong emphasis on the bireosteum, isn't it?
You mentioned it earlier. Yes, he comes back
to it again and again. Why is this membrane...
covering the bone so central to his argument,
particularly when comparing open surgery to closed
methods? Precisely. The periosteum is this layer
of connective tissue covering the outer surface
of most bones. It has an inner layer containing
cells that are crucial for bone formation, osteoporgenitor
cells they're called. Bone forming cells. Essentially,
yes. And Churnley places immense importance on
it because he views it as a site with a remarkably
free and active blood supply. That makes it a
powerhouse for generating callus. Callus is the
body's natural biological cement, you know, the
new bone tissue that bridges the fracture gap
and eventually forms a solid union. Right, the
bulge you sometimes see on x -rays. That's often
it, yes. And in contrast, the vitality of the
periosteum would... the fractured bone ends themselves,
especially in the shafts of long bones in the
cortical bone. Why especially there? Because
a primary blood supply in cortical bone runs
longitudinally through tiny channels called aversion
canals. When a fracture occurs, that longitudinal
supply is interrupted right at the break. Ah,
so the very ends lose their direct supply. Effectively,
yes. His figure 13 in the book is very illustrative.
It seems to show vigorous new bone growth arising
from the periosteum, while the fractured bone
end itself looks almost, well, inert by comparison
in the early stages. Inert? That's a strong word.
It is. He's making a strong point about where
the biological activity is primarily coming from
initially. And he talks about a shibalef. regarding
period steel callus. What was the debate, the
sort of ingrained belief that he was challenging
there? Ah yes, the shibboleth. It's an old belief
for custom, often outdated. Okay. This referred
to a significant philosophical divide amongst
surgeons of the time. One prominent view often
associated with proponents of rigid internal
fixation, like Lane and Sherman earlier in the
century. The pioneers of plates and screws? Exactly.
They saw extensive periosteal callus formation
that bulge, we mentioned, as a sign of inefficient
healing, almost a pathological response. Why?
They believe that ideal union should happen directly
between the perfectly coapted bone ends, what's
sometimes called primary bone healing, though
the understanding of this was still developing.
End -to -end healing, a minimal external callus.
That was the ideal they were aiming for. They
observed that after open reduction, where the
bone ends were meticulously exposed and stripped
of periosteum to achieve perfect anatomical alignment
and apply plates. There seemed to be less visible
periosteal callus on the x -ray afterwards. And
they interpreted this absence of callus as evidence
that their technique was achieving this ideal
inter -end union. But Charley disagreed. Veemently.
He argues completely against this interpretation.
He insists that the early fluffy hazy periosteal
callus looking like a cloud on the x -ray as
shown in his figure 20a is actually a sign of
healthy vigorous biological repair. So a good
sign. A very good sign in his view and he claims
it is never seen after open reduction where the
periosteum has been deliberately stripped away
as in figure 20b. He argues that stripping the
periosteum removes or severely compromises this
vital source of early callus formation. So the
surgical technique aimed at perfection on the
x -ray was, according to Charnley, actually interrupting
a fundamental biological pathway for natural
healing. Precisely his point. And this ties directly
into his deep concern about sepsis infection
in operative fracture treatment. He argues that
stripping the periosteum abolishes the vitality
of the bone surface. It damages its local blood
supply and removes those crucial bone -forming
cells. This creates an environment highly favorable
for infection to take hold and persist, especially
when you introduce a metallic foreign body like
a plate or screws right into that site. Makes
sense. He suggests that many cases of delayed
union or non -union following internal fixation
in that era might actually have been due to deep,
perhaps low -grade infection that later subsided,
but which had rendered the stripped ischemic
bone surface essentially lifeless, preventing
it from participating properly in the healing
process. Lifeless. That's a chilling. This is
where he brings in those rather morbid but incredibly
powerful historical examples, isn't it? John
Hunter's specimens from centuries earlier. Yes,
it's a remarkable rhetorical move, isn't it?
A leap back in time to make a crucial point about
the present was present in 1950. What were these
specimens? He discusses John Hunter's specimens
from the late 18th century. Specifically, these
things called coronet or ring sequestra found
in old infected amputation stumps. Sequestra?
A sequestrum is a piece of dead bone that has
become separated from the surrounding healthy
bone during necrosis. Okay, so dead bone rings
and amputation stumps. Yes. Charlie argues that
an amputation is essentially the proximal half
of a compound fracture. The bone end has been
cut and exposed. In infected stumps from that
era, a ring of dead bone often formed right at
the cut end. And his interpretation? He interprets
this as a zone of cortical bone that was made
discemic, losing its blood supply, both by the
saw cut, which interrupts the longitudinal supply
in the reversion canals, and by the surgical
stripping of the periosteum, which was standard
practice. If infection then sets in, this already
compromised ischemic bone becomes irreversibly
killed. A double whammy. Exactly. These specimens,
preserved for nearly 200 years, served as vivid
evidence for Charnley of the futility of expecting
the ends of cortical bone to join when they're
coapted or compressed together under conditions
where their vitality is compromised. So trying
to force dead ends together won't work? Essentially.
They show that while callus might form externally,
maybe from deeper tissues or surviving periosteum
further away, it cannot reach or incorporate
a truly ischemic bone end. It's a stark demonstration
of how stripping the periosteum, especially with
infection, can turn a living structure capable
of repair into something like, well, he provocatively
describes it as inert mineral substance. Inert
mineral substance? Wow, that connection. Spanning
centuries using anatomical specimens to argue
a point about contemporary surgical technique.
It really underscores his analytical approach,
doesn't it? It absolutely does. He's thinking
biologically, historically, mechanically. So
if these cortical bone ends can become almost
inert, particularly after stripping an infection,
how does successful healing actually occur in
the shafts of long bones, according to his view,
if the ends aren't the main players initially?
This leads into his principles of union. And
distinguishing between different bone types is
key here. Cancellous bone, the spongy bone found
at the ends of long bones near joints that has
a rich, profuse blood supply. That type of bone
heals rapidly, particularly with compression.
Cortical bone forming the dense shafts is different.
As we mentioned, its blood supply is primarily
longitudinal through those narrow aversion canals.
At the moment of fracture, a significant portion
of the cortical bone right at the break is functionally,
well, almost inert mineral compared to the truly
living cellular elements elsewhere. So what needs
to happen? For normal healing in cortical bone,
these aversion vascular channels need to enlarge.
The dense cortex needs to become more porous,
biologically active, allowing blood vessels to
penetrate from the surrounding healthy areas
and bring in healing cells. Like opening up pathways.
Exactly. And Charlie, citing the work of Ham,
another researcher shows how stripping the periosteum
severely impedes this necessary process of vascular
channel enlargement and cortical remodeling.
The bone ends remain dense, less biologically
receptive. So stripping hinders the bone's own
ability to prepare for healing. That's the argument.
This insight is fundamental. For cortical bone,
the biological factors, the vascularity, the
health of the periosteum are paramount. Perhaps
even more so than the purely mechanical act of
rigidly holding the ends together, at least initially.
Which supports his case for conservative treatment
first. It supports his argument for potentially
delaying operative treatment in many cases. allowing
biological recovery and callus formation to begin
under less invasive conservative management first,
preserving that crucial biology. That really
challenges the intuitive idea that you just need
to hold the pieces together tightly as soon as
possible. He's saying the biology has to be right
first. The biology is king, in his view, for
cortical bone healing. And he uses these powerful,
even quite blunt, propositions to compare operative
and conservative methods from his perspective
in the 1950s. Yes, he doesn't pull any punches
at all. His propositions are quite stark. What
are they? First, operative treatment is potentially
harmful to all fractures in the sense that it
introduces inherent risks like infection and
disruption of biology. Conservative treatment...
in contrast, is harmful only to a few fractures
or patients, those where it's clearly unsuitable
or perhaps mismanaged. So surgery is always risky,
conservative only sometimes. That's the gist
of the first point. Second, the few cases harmed
by conservative treatment might have been less
harmed by operation. But he suggests this is
debatable and actually quite hard to prove definitively.
Right. And third, perhaps most critically, the
failures resulting from operative treatment.
and those from conservative methods, are not
equally capable of being salvaged by secondary
procedures. Not equally salvageable. He called
this the critical point. His view is that complications
from operative treatment, especially severe deep
infection involving metalwork and dead bone,
well, they could be catastrophic. far more difficult,
if not impossible, to recover from. Compared
to. Compared to the issues typically encountered
with conservative management, like maybe delayed
union or some degree of deformity, these might
still be addressable with safer, less invasive,
later procedures like bone grafting, which we'll
come to. So it's a calculation of risk versus
reward, prioritizing salvageability over the
potentially disastrous consequences of an early
risky intervention. It's about avoiding burning
bridges, essentially. That's a very good way
to put it. Avoid burning the biological bridges.
And building on this idea of trusting biology
and prioritizing the less destructive approach,
he loops back to the art of closed reduction
and that soft tissue concept you introduced earlier.
Yes, he dedicates significant space to explaining
the mechanics. of closed reduction. He considers
it an art, requiring the surgeon to build accurate
mental pictures of the injury and the surrounding
anatomy. Not just looking at the x -ray. Not
just staring at the x -ray shadows, no. He reiterates
that supreme importance of the soft tissues.
The broken bone fragments are, in a sense, just
indicators. The real guide to reduction lies
in understanding the state of the damaged and,
crucially, the undamaged soft parts. The intact
ligaments, muscles. Exactly. Intact ligaments,
joint capsules, or strips of periosteum can act
as a strong guiding hinge. Like his jigsaw puzzle
analogy for the Potts fracture. You mentioned
that. Exactly that analogy. A Potts fracture.
A common ankle fracture, often involving the
malleoli, those bony bumps on either side, and
ligament tears. It can look like a bewildering
mess of bone fragments on an x -ray. Trying to
reduce it by focusing only on aligning the bones
feels, he says, like trying to solve a jigsaw
puzzle in the dark. The key is to appreciate
which soft tissues are still intact. If you can
manipulate the ankle to restore the normal relationship
of the parts still held together by these intact
ligaments or capsule, the bones will often naturally
follow. He has a model for this, doesn't he?
Yes, a simple but effective model of two pieces
of wood joined by a leather strip. It shows how
this soft tissue hinge works. You can manipulate
the pieces, perhaps even applying forces that
initially increase the deformity slightly to
put tension on the hinge of the leather strap.
This tension then guides the bone, ends back
into alignment, and can even create compression
at the fracture site when the hinge is taut.
Figure 41 illustrates this visually, and figure
44 provides clinical x -ray evidence in a slipped
epiphysis, a growth plate fracture, showing the
periosteum ossifying on the concave side of the
deformity, acting as a biological tether. It
sounds like reduction isn't just about brute
force or simply pushing bone fragments around.
It's about understanding and leveraging the remaining
biological structure. Precisely. It's finesse
guided by anatomical understanding. And this
applies to traction methods as well, pulling
on the limb. Fundamentally, yes. Traction, whether
it's skeletal traction applied through a pin
in the bone, or just skin traction with tapes.
It works by creating tension in the surrounding
soft tissues. OK. This tension helps to pull
the displaced fragments back towards their normal
length and alignment. Continuous traction, like
that used traditionally in a Thomas splint for
a femur fracture, provides what he calls relative
fixation. Yes, it's rigid and holds alignment
when the tension is maintained. but it allows
some flexibility or movement if the tension is
released or overcome. He uses the analogy of
a chain and tension. Interesting. He mentions
his wartime experience influencing his views
on traction. He does. He initially favored fixed
traction to absolutely prevent any distraction
or pulling apart of the fragments, but later
he accepted that balanced traction using weights
was effective too. He concluded that the harm
originally attributed to weight traction ought
to be transferred to the rupture of the pathways
which conduct osseous union. Meaning? Meaning
it wasn't the gentle distraction itself that
was the main problem, but rather using excessive
or inappropriate force that could tear those
vital soft tissue pathways needed for healing.
The biology again. What counteracts this traction,
making it difficult to achieve length sometimes,
even under anesthesia? Is it just muscle spasm?
Muscle tone is certainly a factor, but Charnley
argues it's often not the most significant barrier,
especially in the acute phase. What is, then?
He highlights what he terms a hydraulic element
in limbs that are grossly swollen with large
effusions of blood and fluid. Hydraulic? Yes.
The fibrous compartments within the limb become
distended, intense, like an overinflated tire.
This resists any attempt to lengthen the limb.
The limb naturally tends to adopt a more spherical
shape, which holds the greatest volume for a
given surface area, but corresponds to a shorter
overall length. So the swelling itself fights
against the traction. Exactly. Allowing time
for this acute swelling to subside naturally
can significantly facilitate reduction later
on. Anything else resisting traction? Yes, there's
also resistance from interlocking soft tissues
or sometimes even interlocking jagged bone fragments.
Someone called Beveridge Moore demonstrated experimentally
that sometimes you might need to slightly increase
the deformity or angulation of the fracture first.
Increase it? Why? To unlock the fragments before
applying traction. Applying violent excessive
traction before unlocking or addressing that
hydraulic swelling could actually be harmful
by rupturing those remaining intact soft tissue
strands, the very hinges you were relying on
for guidance and stability. He suggests this
mechanism might even contribute to non -union
in some cases. So the art of closed reduction
involves not just mechanical forces, but a deep
understanding of the limb's soft tissue envelope,
its biological response like swelling, and the
delicate balance required to leverage the body's
inherent structures for healing. It's quite complex.
It's deceptively complex, yes. It requires real
thought and feel, not just brute strength. It
really transforms your understanding of fracture
healing, doesn't it? Charnley isn't just talking
about bones. He's arguing that the invisible
elements, the vitality of the periosteum, the
guiding tension of intact soft tissues, the complex
biological response to injury are fundamentally
more important than simply forcing broken bone
ends together. That's the core of his argument
about biology. It's a powerful reminder that
biological systems heal themselves, and sometimes
our interventions need to respect and facilitate
that process rather than override it. Well said.
That was a truly foundational exploration. Let's
transition now, maybe take a breath, and move
into our second deep dive segment. We'll examine
some specific techniques, challenges, and common
fracture examples through the lens of Charnley's
principles. You mentioned the three -point plaster
system earlier. Could you elaborate a bit more
on the practical application? How does a surgeon
actually create these three points of pressure
to maintain alignment when they're putting the
cast on? Certainly. The three -point system is
really where the art of plaster molding comes
into play. It's not just wrapping. Right. When
applying the wet plaster bandage, the surgeon
needs to actively mold it around the limb with
her hands to create specific indentations and
points of counter pressure. Can you give an example?
OK, say you have a forearm fracture that tends
to angulate to bend in one direction. You would
mold the plaster to press firmly on the limb
below and above the fracture site on the side
it's bending towards. OK, two points. And then
you'd apply firm counter pressure with the heel
of your hand on the opposite side of the limb,
usually right over the apex, the peak of the
fracture bend. The third point. Exactly. It's
this skilled manual pressure applied while the
plaster is still wet and hardening that builds
this internal framework of forces within the
cast, forces that resist the deforming tendency
of the muscles or gravity. Which is why you said
sometimes a curved plaster holds a straight bone.
Precisely. To correct an angulation, you might
deliberately mold the plaster into a curve, even
though the bone inside is meant to be straight.
The plaster's shape dictates the forces it exerts
internally. And this is why he argues the difference
between padded and unpadded plaster is just a
matter of degree in terms of immobilization.
Not a fundamental difference. Exactly. Whether
you have a layer of padding underneath or the
plaster is applied directly to the skin, perhaps
over a thin stockinette, the principle remains
that the plaster is essentially conforming to
and fixed to the skin. And since the skin is
mobile relative to the underlying skeleton, the
bone, as we established, any movement of the
skin translates into some degree of potential
movement at the fracture site, even within the
tightest cast. An unpadded skin -tight cast minimizes
this movement more than a padded one. Sure, it
provides a greater degree of relative immobilization,
reducing that microscopic motion. But neither
is truly rigid. Neither achieves the absolute
zero -motion rigidity of internal fixation, which
directly stabilizes the bone fragments themselves.
This distinction is absolutely key. Plaster provides
relative immobilization, which is often sufficient
for many fractures to heal perfectly well, but
it's not truly rigid in an engineering sense.
And that distinction seems particularly relevant
when he discusses walking plasters, especially
for foot fractures. You were quite emphatic earlier.
Yes, his views on walking plasters for fractures
in the tarsus, the ankle bones of the metatarsus,
those long bones in the foot leading to the toes
are quite definitive. He argues that expecting
a plaster to rigidly immobilize these fractures
while the patient is actually walking on the
foot is, well, he uses the word futile. Futile.
Strong stuff. Why? Because as weight is applied,
the soft tissues of the sole compress significantly.
The arches of the foot flatten or deflect. There's
inherent flexibility and movement within the
foot structure itself. Right. And this movement
translates to movement at the fracture site,
regardless of the outer plaster shell. It can't
prevent that internal deformation under load.
He observes that patients with these fractures
instinctively walk on their heel initially anyway.
Protecting the front of the foot. Exactly. They
effectively use the walking plaster more like
a protective boot to shield from direct knocks
rather than as a rigid splint for the fracture
site itself. So the common fear then that a fracture
will inevitably displace further or get worse
if it's not rigidly splinted, that isn't universally
true according to Charnley. Not universally,
no. He distinguishes between different fracture
types and locations. For long bone shafts, say
in the thigh or upper arm, with significant leverage
and strong muscle pull, yes, spontaneous increase
in deformity will likely occur if they're left
unsupported. The forces are just too great. But
for many short bones... or certain fracture patterns,
even in long bones where there isn't much muscle
pull across the break. He argues the extent of
tearing of the tough surrounding fibrous tissues
like ligaments or joint capsules is what determines
the maximum possible displacement. So it displaces
initially and then stops? Often, yes. Unless
further significant trauma occurs, the displacement
won't worsen beyond this initial level dictated
by the soft tissue envelope. The role of a splint
or cast in these cases is primarily to prevent
recurrence of the initial displacement after
you've reduced it. Right. Not necessarily to
halt an ongoing inevitable process of worsening
deformity that doesn't actually exist in those
cases. Does he suggest that plaster actually
speeds healing? Or is that another assumption
he challenges? He seems to counter the fear that
a fracture will simply fail to unite, go on to
non -union or pseudoarthrosis without immediate
rigid splinting. He suggests this fear is often
unfounded, particularly in short bones like finger
bones, phalanges, or miniature long bones, where
significant gross movement isn't typically the
main issue limiting union. But there are exceptions.
Important ones. Abs -critical exceptions. He
highlights fractures prone to ischemic necrosis.
Ah, ischemic necrosis. That's where the blood
supply is compromised, leading to bone death.
We touched on this with the periosteam stripping.
Exactly the same principle, but caused by the
fracture itself disrupting key vessels. Key points
to fractures of the scaphoid waist or proximal
pole that's a small bone in the wrist and specific
types of femoral neck fractures high up in the
hip, joint mid cervical or subcapital types as
prime examples. Why those specifically? Because
the anatomy is such that the fracture line can
easily sever the main artery supplying blood
to one of the fragments. This leads to a vascular
necrosis or ischemic necrosis. The bone fragment
dies. Right. Tarnley insists this is a complication
of fracture repair, a failure of biological supply,
and must be distinguished from the healing of
normal fractures where blood supply remains intact.
Are there other sites prone to this? Yes. He
mentions the talus, an important ankle bone,
the medial malleolus, that inner ankle bone,
and sometimes certain fractures near the wrist
in the distal tibia or ulna. So for these specific
ischemia -prone fractures, what's needed? For
these, he states that rigid fixation is essential.
Ah, so here rigidity matters. Yes. But critically,
not necessarily, because it speeds normal bone
healing per se. It's essential because the ischemic
dying fragment needs a completely stable, rigidly
held environment in close apposition to the healthy
living bone on the other side of the fracture.
Why? To allow for slow revascularization. For
new blood vessels to gradually grow into the
dead fragment from the living side, and for the
body to slowly replace the dead bone with new
living bone, a process called creeping substitution.
The host bone needs that absolute stability to
carry out this slow repair and incorporation
process. That's a really important distinction.
Rigid fixation isn't a universal accelerator
of healing, but it's specifically necessary to
create the stable conditions needed to salvage
and revascularize a compromised fragment in certain
predictable locations. Precisely. It's targeted
based on biological risk. What about joint stiffness
after fractures? That's a common problem. He
seems to challenge simple explanations for that
as well. He does. He's very wary of overly simplistic,
mechanistic analogies for joint stiffness. You
know, comparing joints to rusty hinges or engine
bearings that just need lubrication or forcing
to get them moving again. Right. The no pain,
no gain physio approach sometimes. He views joint
stickness after fracture or immobilization as
a process of great biological complexity. It
involves not just the joint surface itself, but
all the surrounding soft tissues, the capsule,
ligaments, muscles, tendons, which can become
scarred, thickened, or adherent to each other,
or the bone. So it's more than just the joint
surfaces? Much more. He discusses Bowler's controversial
teaching from Vienna. Bowler claimed that prolonged
fixation in a skin -tight plaster wouldn't cause
permanent stiffness. Really? If the joints were
placed in an optimum position within the cast,
and crucially, if the patient actively used the
limb musculature within the cast. doing static
muscle contractions. Why would that help? The
theory was that muscle activity helped pump away
swelling and fluid, which was thought to contribute
to the formation of adhesions in scar tissue.
Bowler went quite far with this, claiming patients
could leave his plaster cast with minimal disability,
even perform heavy work while still in casts.
Did Turnley agree? He acknowledges that Bowler's
methods had great content of fundamental truth.
particularly regarding the benefit of early activity
in minimizing stiffness. Many joints do recover
full range over time with mobilization. However,
he notes that Bowler's overall teaching ultimately
failed in practice, not primarily because it
caused permanent stiffness, but because it didn't
eliminate the problem of delayed union in certain
difficult fractures. The biology of bone healing
sometimes trumped the prevention of stiffness.
Interesting balance. What does Charlie see as
the worst cause of stiffness? He points out that
severe sepsis deep infection is the commonest
cause of irreparable permanent joint stiffness
because it leads to such extensive dense scar
tissue formation involving everything around
the joint. Biology again. So just trying to mechanically
force a stiff joint might not be the right approach
if the problem is actually complex biological
scarring. That's the implication. A purely mechanical
view might be insufficient or even harmful. He
gives these striking examples, doesn't he? Like
the elbow and the heel bone, the oscalsis, where
attempting perfect anatomical reduction surgically
seems, in his view, to lead to a worse functional
outcome than a less perfect but more biologically
friendly approach. These are perhaps the most
powerful illustrations of his less is more argument
in specific clinical situations. Tell us about
the elbow first. For complex elbow fractures,
things like Y -shaped fractures of the lower
humerus or certain radial head fractures, Charlie
observes that the elbow almost invariably does
badly after operative treatment. Does badly,
meaning stiff. Stiff, yes, often with significant
loss of flexion or extension. He contrasts this
with the results reported by Eastwood, who treated
complex Y -shaped fractures conservatively with
early mobilization, even accepting some displacement
on the x -ray, yet achieved reasonable function.
Better function despite less perfect anatomy.
That's what the evidence suggested. Charnley
admits that in his own experience, even when
he achieved exact restoration of anatomy surgically
in the elbow, the end result in terms of movement
was often similar to, or sometimes even worse
than, the outcomes from conservative methods.
Why would that be? He concludes that stiffness
in the elbow is likely due more to scarring and
contracture in the soft parts, the joint capsule,
the ligaments, the muscles around the joint,
rather than simply the configuration of the joint
surfaces after healing. Surgery, especially extensive
surgery, inevitably adds more scarring. So the
surgical trauma itself contributes to the stiffness?
That seems to be his interpretation. He even
suggests that excision of the radial head, a
procedure often done perhaps too readily even
for minor crack fractures, might actually delay
mobilization by causing more bleeding and reaction.
Any solutions for elbow stiffness? He proposes
that a single forceful late manipulation under
anesthesia might sometimes be effective for persistent
stiffness after about three months. But he cautions
strongly against repeated manipulations, which
he felt just cause more damage and scarring.
OK. And the oscalis, the heel bone, seems to
be his ultimate case study in overtreatment.
Why was that? He presents the oscalis fracture
as an instructive object lesson in the pitfalls
of aggressive intervention aiming for anatomical
perfection. These are nasty fractures, aren't
they, from falls? Often, yes. Falls from a height.
They're complex, frequently involving crushing
and impacting of the bone, particularly affecting
the crucial joint it forms, with the talus above
it, the submaster -galloid joint, which allows
side -to -side foot movement. And the conventional
wisdom was to try and fix it perfectly. The drive
was often towards restoring the anatomical shape,
but Charnley states unequivocally that attempts
to restore the anatomy of the oscalsis almost
invariably results in a stiff subastrogaloid
joint and a painful subastrogaloid joint. Sift
and painful despite perfect reduction. That was
his observation. He cites the universally poor
results achieved with bowler skeletal traction
technique for these fractures, putting a pin
through the bone and pulling. This often resulted
in delayed consolidation in a distracted position,
pulling the fragments apart slightly rather than
the naturally impacted crushed state. So what
was Charlie's counterintuitive finding? His finding,
based on his observation and experience, was
that early mobilization of the fracture in its
impacted position led to better results. Mobilization,
meaning getting the patient moving. Yes, allowing
the patient to move the ankle and foot gently,
as comfort permitted, effectively walking carefully
on the bruised, slightly collapsed heel bone
with minimal support, perhaps just a protective
bandage or a boot, not rigid immobilization.
Accepting the Deformity Accepting the impact
of deformity. He found this led to faster recovery,
less pain, and better overall function. Often,
this conservative approach made late surgical
fusion of the painful subastragaloid joint unnecessary.
whereas it was frequently required after failed
attempts at anatomical reduction. Why did trying
to reduce it make things worse? He argues that
attempts to pull the fracture out to length often
disrupted areas where fibrous union, the initial
scarring, had already started to occur naturally
in the impacted position. This created cavities
that filled with blood clot in the reduced state,
which actually delayed bony union and increased
scarring right in that critical joint. Fascinating.
Almost like leaving well enough alone was better.
In this specific complex fracture, that seemed
to be the case. He also highlights the negative
psychological impact. If his surgeon gives a
gloomy prognosis for this fracture, which was
common, that could contribute to poor outcomes.
He suggests a more positive approach, encouraging
early function is beneficial both physically
and mentally. That's a powerful argument for
prioritizing function in patient recovery over
chasing anatomical perfection on an x -ray, especially
when the anatomy is complexly shattered. Absolutely.
It's a lesson that resonates beyond orthopedics,
surely knowing when not to intervene too aggressively.
Indeed. The examples of the elbow and oscalces
are profound, really. They challenge that intuitive
assumption that perfect anatomical restoration
automatically equals perfect function. Charnley
shows how disrupting the biological environment
or the natural, albeit imperfect, state of the
injured tissues through aggressive surgery, well,
it can lead to more scarring and worse functional
outcomes than accepting some anatomical imperfection.
but facilitating early biological recovery and
functional adaptation through conservative means.
It's a vital lesson. It is. A lesson in understanding
the intricate relationship between structure,
function, and the body's own healing capabilities.
Beyond these major principles and case studies,
he also includes numerous practical tips on plaster
technique throughout the book, doesn't he? Small
details that reinforce the underlying mechanical
principles we discussed. Absolutely. He gets
right down into the practical how -to of applying
a good cast, which was obviously central to his
practice. Like what? For instance, emphasizing
the need for an end -to -end rhythm when applying
the wet plaster bandages, rolling them on smoothly
and evenly. Why is that important? To ensure
even the thickness at a consistent feel along
the whole functional length of the cast. No weak
spots, no overly thick areas, just good craftsmanship.
Makes sense. Any other examples? Yes, the importance
of molding forearm plasters into an oval cross
section rather than just a round tube. Oval?
Why oval? Well, the bones of the forearm, the
radius, and ulna lie side by side. An oval mold
helps maintain the natural space between them,
the interosseous space, and it facilitates better
control of rotation pronation and supination.
A simple round plaster might tend to squeeze
the bones towards each other, which isn't ideal.
Ah, subtle but important. Very. He also details
techniques like wedging a plaster to correct
any residual angulation after it's set. How does
wedging work? You essentially cut the plaster
almost all the way through on the side towards
which the angulation needs to move the concave
side. Then you open up a wedge -shaped gap by
cutting out a larger piece on the opposite side,
the convex side. Then you manipulate the limb
to close the first cut and open the wedge, correcting
the angle, and hold it there with a new wrap
of plaster. It maintains the three -point fixation
principle. Clever, like fine -tuning the alignment.
Exactly. And he also advises splitting plasters
longitudinally down the side after procedures
like bone grafting. Why split them? To prevent
pain and circulatory compromise due to the inevitable
post -operative swelling. It allows the limb
to swell slightly without the cast becoming dangerously
tight, ensuring the biological healing process
isn't impeded by external pressure. practical
considerations for biological processes. He also
mentions the classic Thomas splint for femur
fracture, still used sometimes today, isn't it?
Less commonly now with modern surgical fixation,
but yes, historically it was a mainstay of conservative
femur fracture management for decades, particularly
valuable during wartime due to its relative simplicity
and effectiveness with either fixed or balanced
traction. What were the challenges with it? He
describes its use and the common issues, such
as managing the pressure from the padded ring
at the groin, which could cause sores. He mentions
using counterpoising techniques to help manage
that. And he reiterates the ongoing debate from
that time around early knee movement while the
femur fracture was healing in the splint. The
stiffness versus healing debate again. Precisely.
functionally appealing to start moving the knee
early to prevent stiffness, but potentially risking
some loss of position or distraction at the fracture
site, or even leading to a late varus deformity,
a bowing of the thigh bone. Always trade -offs.
And wrapping up our look at specific fractures,
the POTS fracture of the ankle, which you said
earlier he seems to approach with a certain fondness.
He does seem to describe the pleasure of reducing
a pot's fracture once you truly understand its
mechanics, contrasting it with the frustration
he felt in earlier attempts before he fully grasped
the principles involved. And it's a prime example
of the soft tissue hinge concept. Absolutely.
He stresses that in the common type of injury,
an external rotation type, the ligaments on the
medial, the inner side of the ankle, often remain
intact even if the bones are broken. These intact
ligaments are the key. So how do you use them?
By manipulating the foot, often using gravity
or a specific support position, perhaps an internal
rotation, and some supination turning the sole
inwards and maintaining pressure, you can leverage
these intact structures, put tension on them,
to guide the talus, it's the main ankle bone
that sits above the heel bone, back into its
proper relationship underneath the tibia, the
main shin bone. And the broken dits follow? And
the fractured malleoli, the bony knobs, will
generally follow the talus back into a good position.
He notes that slight displacement of the posterior
malleolus, the back part of the tibia at the
ankle joint, is often acceptable. Even if it's
not perfectly aligned? Yes. If the main ankle
joint itself, the relationship between the talus
and the tibia, is well reduced and stable. Again,
favoring functional alignment of the main weight
-bearing joint over perfect anatomical alignment
of every single fragment. And traction isn't
usually needed here. Skeletal traction is rarely
needed for these ankle fractures, in his view,
if the manipulative technique based on understanding
the soft tissues is mastered. It's clear this
book is just a masterclass in observation, mechanics,
and challenging assumptions, isn't it? Drawing
on history from Hippocrates' ancient principles
of reduction right up to John Hunter's specimens
to inform contemporary practice. It really is
a synthesis of observation, biomechanics, and
historical perspective. And it's perhaps fitting
that Charnley's later, arguably more famous work,
the development of the modern low -friction hip
replacement. Well, that work is associated with
the John Charnley Trust's pioneering emphasis
on decades -long patient follow -up, 30 -year
follow -up as a gold standard. It reflects that
same commitment to rigorous long -term evaluation
of outcomes that he implicitly advocates for
when discussing the difficulties of comparing
treatment methods right at the start of this
book on fractures. A very consistent philosophy
throughout his career, yes. That was a truly
expansive deep dive, covering fundamental biology,
practical mechanics, specific fracture examples,
all through the lens of a classic text that really
challenges us to think critically. Let's try
and distill some of the core ideas in a quick
lightning round. Ready? Ready. First, name one
key anatomical structure, Charnley emphasizes
as being more important than the bone fragments
themselves in successful closed reduction. The
intact soft tissues ligaments, periosteum acting
as a hinge or guide. According to the book, what's
a key biological risk associated with stripping
the periosteum during open surgery? It compromises
the blood supply to the bone surface, damages
its vitality, and increases the risk of persistent
sepsis, which impedes callus formation. What's
the striking counterintuitive finding from the
book regarding the treatment of severe heel bone,
os calcis, fractures? That early mobilization
in the impacted position, excepting the deformity,
often yields better functional results than attempts
at anatomical restoration or using traction.
Churnley describes something as the greatest
advanced intibial fracture treatment in the 50
years prior to his writing. What was it? The
Femister bone graft technique applying thin slices
of the patient's own bone onto the surface of
a delayed union site to stimulate healing. A
concept challenging the idea that a plaster cast
provides absolute rigidity. The three -point
system combined with the principle of relative
immobilization limited by the movement between
the skin and the skeleton. And finally, beyond
anatomy and mechanics, what did Charnley suggest
contributed negatively to outcomes in those difficult
lost calcis fractures? The surgeon's own gloomy
attitude towards the injury, which he felt could
negatively impact the patient's psychological
state and potentially hinder their recovery.
Those quick points really highlight the sheer
range of insights in this book. Let's finish
now with some actionable takeaways, maybe some
universal principles that we can draw from this
deep dive into Charlie's classic text, things
that apply more broadly perhaps. Yes, I think
looking at this book. several core principles
really stand out that apply well beyond the field
of orthopedics, actually. Absolutely. For me,
one is the fundamental importance of understanding
the underlying principles and mechanics of any
system, whether it's bone healing or, you know,
a complex business process, rather than just
blindly following routine protocols. Charnley
constantly probes the why. Definitely. And tied
right into that is the value of challenging conventional
wisdom, resisting overly simplistic explanations
for complex biological or systemic problems.
We saw that with joint stiffness, it isn't just
mechanical. Financial markets aren't purely rational
either. Biological systems, social systems, they
have inherent complexity that demands a deeper
look. And recognizing the critical role of those
often invisible factors. The soft tissues, in
his case, the blood supply, the periosteum, the
biological vitality, things that don't show up
easily on initial stands or simple analyses,
but are absolutely fundamental to the system's
function and repair. Looking beyond the obvious
data points. Another significant lesson, I think,
underscored by Charlie's own career and the legacy
of his trust with the hip replacements, is the
importance of long term outcomes and careful,
prolonged observation. True evaluation of any
treatment, any strategy, any intervention requires
patience and assessment far beyond just the immediate
results. We need the long view. So true. And
finally, that recurring powerful theme, sometimes
less is more. Recognizing when overtreatment
or excessive intervention might disrupt a system's
natural ability to recover or adapt and could
lead to unintended negative consequences. That's
a crucial skill, isn't it? Whether you're fixing
a bone, managing a team, or designing a product.
Knowing when not to interfere aggressively can
be just as vital as knowing when to act. Finding
that balance. And, you know, revisiting these
foundational texts like Charnley's allows us
to see how brilliant minds grappled with complex
problems using the tools and knowledge of their
time. It reminds us that the principles they
uncovered through careful observation often hold
enduring truth. It really does. It encourages
us to be critical thinkers ourselves, I think.
Always questioning assumptions and looking deeper
than the surface. A truly thought -provoking
point to leave you, our listeners, with. If you
found this deep dive insightful, perhaps consider
sharing it with a colleague or friend who enjoys
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genuinely helps us reach more curious minds like
yours. It does indeed. That's all for this deep
dive into the foundational principles of fracture
treatment, inspired by John Charnley's classic
text. Thank you for joining us. You can find
more deep dives wherever you get your podcasts.