Latest / Deep Dive Ortho — Orthopaedic Surgery, AI & Digital Health Podcast. / Bone Metastasis and Skeletal Disease Management

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Bone Metastasis and Skeletal Disease Management · Deep Dive Ortho — Orthopaedic Surgery, AI & Digital Health Podcast.

0:00
Welcome back to the Deep Dive. Today, we're tackling
0:02
a challenge that, well, it's becoming increasingly
0:04
common and certainly has a huge impact in orthopedic
0:07
practice. We're talking about managing patients
0:08
with advanced cancer, where bone pain and the
0:11
risk of pathological fractures really come to
0:13
the fore. And it's more than just treating a
0:15
symptom, isn't it? It's about navigating this
0:17
really complex sort of evolving landscape. Precision
0:20
in diagnosis, in management, it's absolutely
0:23
critical for us as mid -senior medical professionals.
0:25
So our mission today is to really unpack the
0:27
intricacies of metastatic bone disease, focusing
0:30
on how it affects the limbs. We want to pull
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out those essential insights that directly shape
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patient care and, crucially, their quality of
0:37
life. And guiding us through this challenging
0:40
clinical terrain, we're incredibly fortunate
0:42
to have Professor Mor Imam with us today. His
0:45
expertise will really help eliminate these often
0:47
quite daunting scenarios. Hashtag, tag, tag,
0:50
understanding the landscape of bone metastasis.
0:52
So just to set the scene, could you start by
0:54
clarifying what exactly we mean by metastatic
0:57
bone disease? How does it really differ from
0:59
primary bone cancer? And why is that distinction
1:02
just so important in clinical oncology today?
1:04
Yes, absolutely. It's a crucial starting point.
1:07
Metastatic bone cancer, or as we often call it,
1:10
secondary bone cancer. Well, it describes tumors
1:14
that start somewhere else in the body and other
1:15
tissues or organs, and then they spread, they
1:18
metastasize, to the bone. Right, so originating
1:21
elsewhere. Exactly. And that's the key difference
1:24
from primary bone cancer. Primary bone cancer
1:26
actually develops from cancerous bone cells within
1:29
the bone itself. It's a much, much rarer diagnosis,
1:32
comparatively speaking. Now, the significance
1:34
of metastatic bone disease really lies in its
1:36
prevalence. The skeleton is, believe it or not,
1:39
the third most common place for metastatic disease
1:41
to land right after the lung and the liver. Third
1:43
most common. Wow. Yes. And part of the reason
1:46
is the bone's very rich arterial supply. It makes
1:49
it, well, a very receptive environment for those
1:52
tumor cells circulating in the blood after breaking
1:54
off from the primary site. It's also vital to
1:56
grasp that this isn't one single disease. It's
1:59
a huge heterogeneous group. But despite the variety,
2:02
they often do respond to different treatments.
2:05
Chemotherapy, radiation, sometimes surgery. The
2:09
overall goal always is to manage the significant
2:12
clinical challenges it throws up, challenges
2:15
that directly and often quite severely impact
2:18
a patient's quality of life. That really clarifies
2:20
it, common and impactful. So digging in a bit
2:22
more, where do these secondary bone cancers typically
2:25
come from, and what do the numbers tell us about
2:27
incidence and maybe more starkly about patient
2:30
survival? Well, historically, and it still holds
2:32
true. The most common origin is carcinomas. So
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we most frequently see this coming from primary
2:37
tumors in the breast, the lung, and the prostate.
2:39
Those are the big three. But we are seeing more
2:42
arising from renal cell carcinoma, that's kidney
2:44
cancer, and also thyroid cancer. And they often
2:47
have quite distinct patterns when they spread
2:49
to bone. It's also worth mentioning non -epithelial
2:52
cancers. Things like hematologic malignancies,
2:55
multiple myeloma, lymphoma, they can... definitely
2:58
involve bone, and sarcomas too, though they typically
3:01
metastasize to bone quite late in the disease
3:03
course. And the survival figures, I imagine they
3:06
vary quite a bit. They vary dramatically, and
3:08
that's critical when we're talking to patients.
3:11
For instance, someone with lung cancer that spread
3:13
to bone. Unfortunately, the median survival is
3:15
typically around six to seven months. Oh, that's
3:18
tough. It is. Compare that to breast cancer,
3:20
where median survival might be 19 to 25 months,
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maybe a 20 % five -year survival. Prostate cancer
3:25
has a wider range too, perhaps 12 to 53 months
3:28
median survival, five -year survival around 25%.
3:31
Myeloma, about 20 months median, 10 % of five
3:34
years. Kidney cancer, often aggressive, maybe
3:37
six months median, 10 % of five years. Thyroid
3:40
cancer though, often slower growing, stands out
3:43
48 months median survival, 40 % of five years.
3:46
A huge difference there. Absolutely. And melanoma,
3:49
again, often aggressive, about 6 months median,
3:51
only 5 % surviving 5 years. So the variability
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is striking. In terms of overall incidence, one
3:57
big U .S. study estimated about 2 .9 % cumulative
4:00
incidence at 30 days, rising to 8 .4 % by 10
4:03
years. Prostate cancer carries the highest risk,
4:06
somewhere between 18 % and 29%, then lung, renal,
4:10
breast. And clinically, how patients present
4:12
also varies. It might be just a single bone lesion
4:14
or what we call oligometastatic disease, just
4:16
a few spots, or it could be multiple bone metastases
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or even metastases in bone plus other organs
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like the liver or lungs. This variety really
4:24
underlines why we need a tailored approach for
4:26
each patient. Hashtag tag tag the mechanisms
4:28
of spread and bone damage. It is quite remarkable
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how these cancers, starting so far away, find
4:33
their way to bone. What is it about bone specifically
4:35
that makes it such a, well, receptive spot? And
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can you walk us through the actual mechanisms
4:39
of how they spread? It is remarkable, you're
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right. And the process is often explained by
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this concept called the seed and soil hypothesis.
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Basically, successful metastasis isn't just random
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chance. It depends on the specific characteristics
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of the tumor cell, the seed, and a very receptive
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microenvironment in the bone, the soil. The main
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way they get there, overwhelmingly, it's hematogenous
5:01
spread through the bloodstream. Although, you
5:04
can also get local invasion, where a soft tissue
5:07
tumor nearby just goes directly into the adjacent
5:09
bone. Now, if we look at spinal metastasis specifically,
5:13
spread via the venous system is really dominant.
5:15
Think about lung and breast cancer. They often
5:17
go to the thoracic spine. Why? Because of their
5:20
venous drainage. Breast cancer drains via the
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ozygous vein, which talks directly to Batson's
5:25
plexus in the spine, a network of veins without
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valves. I have a direct route. Exactly. And similarly,
5:32
prostate cancer often goes to the lumbar sacral
5:34
spine and pelvis because its drainage is via
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the pelvic plexus there. It's anatomy facilitating
5:39
the spread. Interestingly, lung and renal cancer
5:42
can sometimes spread way out to the distal extremities,
5:45
hands, feet. That's often thought to be via the
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arterial tree, indicating more widespread systemic
5:50
seeding. But coming back to seed and soil, once
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those tumor cells arrive in the bone marrow,
5:56
really complex interactions happen. Tumor cell
5:58
receptors Things like CXCR4 and Aran -KL, they
6:02
interact with the bone marrow stromal cells and
6:05
the bone matrix itself. And that interaction
6:07
is key. Absolutely pivotal, because it triggers
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a whole cascade. It leads to the release of growth
6:11
factors, cytokines, things like interleukin 6,
6:13
interleukin 8, and factors that promote blood
6:15
vessel growth, like VEGF. So the cancer cells
6:18
are manipulating the local environment. Precisely.
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This biochemical soup drives tumor growth. But
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critically, it also activates osteoclasts. the
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cells that break down bone leading to osteolysis,
6:30
the destruction of bone. So the cancer cells
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effectively hijack the bone's own regulatory
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systems to create an environment that helps them
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thrive and spread. They coerce the bone into
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supporting their own destructive agenda, in a
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way. That's quite an insidious mechanism actively
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manipulating the bone. So given this manipulation,
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how do the metastatic cells actually impact the
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bone structure itself? Do they manifest differently?
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And what are the cellular processes driving this
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destruction or maybe sometimes, surprisingly,
7:00
new bone formation? That's exactly right. They're
7:02
active players. And when we look at imaging,
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we broadly classify how they affect the bone
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into three main types based on appearance and
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the underlying cellular chaos they cause. First,
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you have osteoblastic lesions, also called sclerotic.
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These are characterized by new bone formation,
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although it's often disorganized. You see this
7:19
most classically in prostate cancer. About 90
7:21
% of prostate mets are blastic. Breast cancer
7:24
can also show blastic features, maybe 60 % of
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the time. So they actually make bone grow. In
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a way, yes. The tumor cells secrete a molecule
7:32
called endothelin 1, ET1. This binds to receptors
7:36
on osteoblasts, the bone building cells, stimulating
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them, and activating pathways like the WNT pathway,
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it promotes new bone formation. It's almost like
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the tumor is tricking the bone into building
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a scaffold around it. Second, we have osteolytic
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lesions. These are all about bone destruction,
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very common in breast, lung, and renal cancers.
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In fact, lung, thyroid, and renal mets are predominantly
7:58
etolytic. On imaging, you see thinning of the
8:00
bone's internal structure, the trabeculae, often
8:03
with fuzzy, ill -defined margins. It looks like
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the bone is being eaten away. And thirdly, you
8:08
get mixed lesions, showing features of both destruction
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and new formation. You see this frequently in
8:13
breast cancer, highlighting its complex interaction
8:15
with bone. Okay. And you mentioned osteolytic
8:17
lesions destruction. What's driving that specifically?
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Ah yes, this is where we get into what's called
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the vicious circle of bone destruction. It's
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a really key concept. It starts with tumor cells
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secreting a protein called PTHRP, parathyroid
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hormone related protein. This PTHRP stimulates
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osteoblasts to release another key molecule,
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NKL. NKL then binds to its receptor, rank, which
8:40
sits on osteoclast precursors. This binding signals
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these precursors to mature into active osteoclasts,
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the bone destroyers. Right, the cells that break
8:49
down bones. Exactly. So these activated osteoclasts
8:52
get to work, causing significant bone resorption,
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breaking down the bone matrix. But here's the
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vicious part. As the bone breaks down, it releases
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growth factors stored within it, things like
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TGF beta, ILGF -1, and calcium. These released
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factors then feed back and stimulate the tumor
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cells to produce even more PTHRP. Ah, so it literally
9:11
feeds itself a cycle. Precisely. It perpetuates
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and accelerates the cycle of bone destruction
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and tumor growth. Plus, other pro -inflammatory
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cytokines like IL -6 and IL -8 and VEGF also
9:22
contribute further fueling the fire. It's a really
9:24
destructive feedback loop. That vicious circle
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sounds incredibly damaging and you can see how
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it leads to so much pathology. So with this destructive
9:33
process happening at the cellular level, how
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does it actually show up in a patient's life?
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What are the key clinical signs, those red flags,
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that should really make us think about metastatic
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bone disease? And what are the critical skeletal
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-related events, SREs, that we absolutely need
9:50
to be watching out for? Well, the most common
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way patients present is almost always with progressive
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pain or the development of one of these skeletal
9:57
-related events, SREs for short. It's actually
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quite common for patients, especially if they're
10:01
still active, to initially blame the symptoms
10:03
on some unrelated knock or a low energy injury.
10:06
Oh, I must have just pulled something. Irrationalize
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it. Exactly. But a classic red flag for us is
10:12
pain that just doesn't go away, maybe even gets
10:15
worse, despite standard painkillers. That suggests
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something more serious is going on. A thorough
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history and physical exam are absolutely vital
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for spotting specific red flags. We're looking
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for things like night pain, often described as
10:28
this dull, boring ache, comes on gradually, characteristically
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worse at night, sometimes waking them up. It
10:35
is. Unintentional weight loss is another big
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one. Pain, specifically with weight bearing,
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especially if it's new or worsening, is very
10:43
concerning for mechanical instability. And of
10:45
course, finding and enlarging mass in the area
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is a direct sign needing urgent investigation.
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Clinicians should look carefully at the skin
10:52
over the area any sweating, tenderness on palpation,
10:56
open wounds, even dimpling. And if you suspect
10:59
an impending fracture or they've had an injury,
11:02
initial immobilization with a simple splint can
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be crucial to stop a fracture propagating. Where
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does it usually happen? The vertebrae are by
11:09
far the most common site. After that, the femur,
11:12
pelvis, ribs, sternum, the top of the humerus,
11:14
and the skull. This distribution often dictates
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the kind of SREs we see. Right, so what are those
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key SREs? Right, the skeletal -related events.
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These are the major problems that arise directly
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from the bone architecture being destroyed. First,
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as I said, bone pain, most frequent symptom.
11:30
It can be mechanical pain from weakened bone
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moving or tuberogenic pain from the tumor itself,
11:35
irritating nerves or stretching the periosteum.
11:39
Next, and this is a huge concern due to a potential
11:41
permanent disability, is nerve root or spinal
11:44
cord compression. Because the spine is the most
11:46
common site, this is a really serious complication.
11:49
It's an orthopedic emergency. An emergency. Absolutely.
11:52
Yeah. Nerve root compression might just cause
11:53
a ridiculous pain, that sharp shooting pain down
11:56
an arm or leg. But spinal cord compression. that
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often starts with back pain, then progresses
12:01
to ling weakness, the second most common symptom.
12:04
You can get sensory changes too, numbness, tingling
12:06
below the level. Late signs are autonomic dysfunction,
12:10
bowel, bladder problems, impotence, that's critical.
12:13
Early recognition, quick workup, urgent surgical
12:15
consultation, they're vital to prevent potentially
12:18
devastating permanent neurological damage like
12:20
paralysis. Then there's hypercalitemia, high
12:23
calcium levels in the blood. occurs in maybe
12:25
10 -30 % of cases with osteolectic mats. And
12:28
unfortunately, it usually signals a poor prognosis
12:30
overall. It's mainly driven by that excessive
12:32
osteoclast activity stimulated by PTHRP releasing
12:36
too much calcium from the bone. And how does
12:38
that present? Symptoms can be vague nausea, poor
12:40
appetite, abdominal pain, constipation, changes
12:43
in mental state like confusion or lethargy, even
12:46
coma. It needs immediate hospital admission and
12:48
IV fluids to bring the calcium down. Pathological
12:52
fractures are another major SRE. The weakened
12:54
bone breaks with minimal or no trauma. Constant
12:57
pain is typical beforehand. Spinal fractures
13:00
are often worse sitting or standing. These fractures
13:02
cause huge problems, severe pain, nerve issues
13:05
like sciatica, the pelvis fractures, deformities,
13:08
immobility. They happen at presentation in maybe
13:11
8 -30 % of patients and crucially, 90 % of them
13:14
need surgery. They almost never heal on their
13:16
own. They don't heal. That's critical for planning.
13:18
Absolutely. We can't rely on biology to fix it.
13:20
And finally, myelophysis. That's symptomatic
13:23
anemia because the metastatic cells infiltrate
13:25
the bone marrow and crowd out the normal blood
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-forming cells. In late stages, you can get pancetopenia
13:30
low levels of all blood cells. All these SREs
13:33
just devastate a patient's quality of life and
13:35
independence, which is why catching things early
13:37
and intervening thoughtfully is so incredibly
13:39
important. That's a really clear picture of the
13:42
clinical impact and just how devastating SREs
13:44
can be. So given all these symptoms and potential
13:47
complications, how crucial is getting an early
13:49
diagnosis? And what are the sort of standard
13:52
pathways and tools we use to confirm metastatic
13:55
bone disease, especially if we don't know where
13:56
the primary cancer is? Early identification is
13:59
absolutely paramount. It's not just for accurate
14:02
staging or predicting prognosis, though that's
14:04
important. It's mainly for getting timely prophylactic
14:07
measures and treatments in place. Doing that
14:09
early can significantly reduce morbidity, prevent
14:12
those awful SREs, and often extend a patient's
14:16
functional life, their quality time. The approach
14:19
really demands a complete workup before any major
14:21
intervention, especially if someone presents
14:24
with a pathological fracture. Because remember,
14:27
that bone metastasis might be the very first
14:29
sign of an unknown primary cancer. We see that
14:31
quite often. Or it could be in someone with a
14:33
known cancer history. So if the primary is unknown,
14:37
or if the patient has a history of multiple different
14:39
cancers, a biopsy is essential. Absolutely essential.
14:43
Before we even think about planning surgery,
14:44
it's a fundamental rule. Don't operate on a bone
14:47
lesion without knowing what it is through a tissue
14:49
diagnosis. That makes perfect sense, biopsy first.
14:52
So once we suspect metastatic disease, what are
14:55
the main imaging tools we reach for? Can you
14:57
walk us through the strengths and weaknesses
14:58
of each one, from simple x -rays up to the more
15:01
advanced nuclear medicine scans? Certainly. Each
15:04
one gives us a different piece of the puzzle,
15:06
and we often use them together to build the full
15:08
picture. Plane radiographs' x -rays are usually
15:11
the first step for someone with focal bone pain.
15:13
We use them to check out suspicious areas seen
15:15
on a bone scan or to look for obvious fractures.
15:18
They're best at seeing osteolytic lesions, the
15:20
destructive ones. But here's the catch. A lesion
15:23
often needs to be quite large, maybe over a centimeter
15:26
or two, and have destroyed over 50 % of the bone
15:29
mineral content before it even shows up clearly
15:32
on an x -ray. So a normal x -ray doesn't rule
15:34
it out then? Not at all. Lytic lesions look like
15:37
areas of decreased density, maybe fuzzy edges.
15:40
Slerotic lesions look denser. more nodular. X
15:43
-rays can help monitor progression or healing.
15:46
Seeing sclerosis increase can be a sign of response
15:48
to treatment, but their main weakness is poor
15:50
sensitivity for early or subtle disease. Computed
15:54
tomography, or CT, is much more sensitive than
15:56
x -ray, maybe around 74%. It gives excellent
15:59
detail of both the cortical shell and the internal
16:01
trabecular bone. Great for seeing both inoculitic
16:04
and blastic lesions. What are the advantages
16:06
of CT? Several. It can help with staging cancer
16:09
elsewhere in the body at the same time. It lets
16:11
us objectively measure bone density changes using
16:14
Houndsfield units, which helps assess response.
16:17
Ribs are much better seen on CT. And it's incredibly
16:20
useful for preoperative planning, especially
16:22
in tricky areas like the shoulder or pelvis.
16:25
We can get 3D reconstructions to guide surgery.
16:27
Magnetic Resonance Imaging, MRI, is really the
16:30
gold standard for looking at soft tissues in
16:32
bone marrow. It has very high sensitivity, around
16:34
95%, and specificity, maybe 90%, for detecting
16:38
bone myths. Better than a bone scan for early
16:40
detection. Yes. A key advantage is it can detect
16:43
marrow involvement before the bone structure
16:45
itself changes enough to be seen as a blastic
16:47
lesion. So it picks up disease earlier. It's
16:51
also safe in pregnancy and absolutely crucial
16:53
for assessing suspected spinal cord compression.
16:56
It shows the relationship between the tumor and
16:58
the nerves perfectly. Metastases typically look
17:01
dark on T1 -weighted images, replacing the bright
17:04
fatty marrow and bright on T2 -weighted images,
17:07
indicating water content like oedema or tumor
17:09
cells. Whole -body MRI is also becoming more
17:12
common, highly accurate for early detection,
17:14
especially in areas rich in red marrow like the
17:16
spine and pelvis. Then we move to nuclear medicine
17:19
scans. These use radioactive tracers that are
17:22
taken up by bone. The skeletal scintigraphy,
17:24
or bone scan, using Technetium 99 -meter MDP,
17:27
is the workhorse. Scans the whole skeleton, very
17:30
sensitive, maybe 78 % for early diagnosis. It's
17:33
great at detecting osteoblastic activity areas
17:35
of increased bone turnover show up as hot spots.
17:37
But it has downsides. Big ones. Low specificity.
17:41
A hot spot could be arthritis, infection, a healing
17:44
fracture, anything causing bone turnover. I can't
17:46
reliably distinguish benign from malignant. And
17:49
it's notoriously poor for purely lytic lesions,
17:52
because there's no increased bone formation to
17:53
pick up the tracer. Myeloma lesions, for example,
17:56
are often cold on a bone scan. Spect imaging,
17:59
also using TC99 -medin -MDP, gives us cross -sectional
18:02
images, like CT. This provides better anatomical
18:05
localization and improves specificity to around
18:07
91 % compared to the planar bone scan. PE scans,
18:11
using tracers like 18F -FDG, glucose analog,
18:14
or 18F -sodium fluorine, NAF, reflex bone production,
18:17
identify METs based on metabolic activity. PD
18:20
generally has better spatial resolution than
18:22
bone scans or SPECT. 18F -NAF -PET, in particular,
18:25
has shown substantially better sensitivity and
18:27
specificity than bone scan and SPECT. It's a
18:29
very powerful tool. And finally, we have hybrid
18:31
imaging. Combining modalities is key. For example,
18:34
18F -NAF -PET -CT fuses the metabolic information
18:37
from PD with the anatomical detail from CT. It
18:39
gives fantastic sensitivity close to 100 % and
18:42
specificity around 97%. You see exactly where
18:44
the metabolic activity is located. Other useful
18:46
hybrids include Spexiti, Petziti, and even PDMRI.
18:51
They all help give us the most complete picture
18:53
to guide diagnosis and treatment. That's a fantastic
18:56
run -through of the imaging toolkit. It really
18:58
shows how layering these techniques gives us
19:00
a clearer picture. Beyond the scans, what about
19:02
lab tests? What blood work helps in the diagnosis?
19:06
And crucially, when is that biopsy absolutely
19:09
essential, especially when the primary cancer
19:11
isn't known? Lab investigations definitely play
19:14
a valuable supporting role, giving us systemic
19:16
clues. Routine bloods like a complete blood count,
19:19
CBC, and a comprehensive metabolic panel are
19:22
standard. The CBC might show anemia, low platelets,
19:26
or even pancytopenia in late -stage disease,
19:29
indicating significant marrow involvement, often
19:31
a poor sign. Serum calcium and alkaline phosphatase
19:34
can be elevated because of the bone destruction,
19:37
the osteolysis. While specific bone turnover
19:39
markers are still researched, things like tartrate
19:42
-resistant acid phosphatase can be high in breast
19:44
and prostate cancer mats. Are there specific
19:46
tumor markers, too? Yes, depending on what primary
19:48
we suspect. Reject PSA for prostate, CA125 for
19:53
ovarian, CA19 .9 for pancreatic biliary, calcitonin
19:57
for medullary thyroid cancer, CEA for colorectal
20:00
or breast, plus thyroid function tests. And it's
20:03
really important to screen for multiple myeloma,
20:05
which can look very similar. So we do serum and
20:07
urine protein electrophoresis, SBEP, UPEP, beta
20:10
-2 microglobulin, C -reactive protein. Even simple
20:13
urinalysis might show blood pointing towards
20:15
the kidney primary. Now, the biopsy. This is
20:18
often where we get the definitive answer, and
20:19
it's absolutely critical. You must get tissue
20:22
confirmation if the patient has an unknown primary
20:24
cancer or if they have a known cancer history
20:26
but haven't had bone meds before. We also strongly
20:30
consider it if someone has a history of multiple
20:32
different cancers. We need to know which cancer
20:34
has spread to the bone to guide the right systemic
20:36
treatment. And what does the biopsy tell us?
20:38
The histopathology. Under the microscope might
20:41
show characteristic features like epithelial
20:43
cells clumped together. Then we use immunostaining
20:46
special stains like keratin, CK7 for breast lung,
20:49
TTF1 for lung to help pinpoint the origin. For
20:52
breast cancer, checking the hormone receptor
20:54
status ER, PR, retinue is essential for guiding
20:58
medical therapy. Imaging, as we discussed, helps
21:01
us pick the best, safest spot for the biopsy
21:03
or guides a needle biopsy accurately. But the
21:06
bottom line, I can't stress it enough, is you
21:08
should not proceed with major surgery on a bone
21:10
lesion without a tissue diagnosis first. It prevents
21:13
mismanaging something else entirely. Such a crucial
21:16
point, tissue, is the issue. So with all these
21:19
diagnostic tools, what other conditions might
21:21
look like bone metastasis? What's the thought
21:23
process for telling them apart, especially when
21:25
things aren't straightforward? That's a really
21:27
important question because the differential diagnosis
21:29
can be quite wide, and it often depends on the
21:32
specific bone involved and the patient's history.
21:34
But the main things we need to rule out include
21:37
primary bone sarcoma, totally different treatment,
21:40
multiple myeloma of the blood cancer causing
21:42
lytic lesions, primary malignant lymphoma bone.
21:46
even secondary sarcoma that can arise after radiation
21:48
treatment years later. And non -cancerous things.
21:51
Absolutely. Osteomyelitis bone infection can
21:54
look very similar with pain and imaging changes.
21:57
Then there are non -tumor conditions like myositis
21:59
ossificans, certain metabolic bone diseases,
22:02
osteonecrosis, especially around the hip, or
22:04
synovial proliferative diseases. So how do you
22:07
differentiate, say, an osteoporotic fracture
22:09
from a metastatic one? That's a common dilemma.
22:13
On imaging, a key difference can be the cortical
22:15
bone. In osteoporosis, the cortex might be thin,
22:18
but is usually intact. With metastatic cancer
22:21
causing a fracture, you often see destruction
22:23
of the cortex itself, a moth -eaten or permeative
22:26
look. But clinically, a low energy injury combined
22:29
with any of those SREs we talked about especially,
22:32
that persistent night pain, weight loss, pain
22:34
on weight bearing that should heavily point you
22:36
towards metastatic disease over a simple osteoporotic
22:40
fracture. The presence of those red flag symptoms
22:43
is really key in steering the diagnosis away
22:45
from benign causes. It's about integrating the
22:48
imaging, the labs, and that detailed patient
22:50
history. Hashtag, hashtag prognosis and risk
22:52
assessment. Understanding the likely prognosis
22:55
is just so vital, isn't it? Not just for our
22:57
planning, but for having honest conversations
22:59
with patients. What are the main factors that
23:02
influence survival when cancer has spread to
23:03
the bone? And how do we actually assess that
23:05
critical risk of an impending fracture? Predicting
23:08
outcomes is indeed a crucial part of management.
23:11
It guides everything we do and how we counsel
23:13
patients. Several things strongly influence survival.
23:17
Simply having skeletal metastases is generally
23:19
a poor sign, but having visceral metastases spread
23:22
to organs like the lung, liver, or brain is even
23:25
worse. The number of metastatic sites also matters.
23:28
More sites mean poorer prognosis. Visceral mets
23:31
are often seen as indicating an irreversible
23:32
stage, shifting our focus much more towards palliation.
23:35
The primary tumor type is a massive factor. As
23:38
we saw with those survival stats earlier, lung
23:40
cancer meds might mean months, thyroid cancer
23:43
meds could mean years. That difference drastically
23:46
changes our treatment intensity. Are there specific
23:48
factors within each cancer type? Yes. For breast
23:51
cancer, things like other non -bone meds, the
23:54
time since initial diagnosis, disease -free interval,
23:57
performance status, hormone receptor status,
24:00
age, and tumor grade all play a role. For prostate
24:03
cancer, performance status, non -bone mets, and
24:06
how markers like alkaline phosphatase and PSA
24:08
respond to treatment are key predictors. In multiple
24:11
myeloma, levels of beta -2 microlobulin and C
24:14
-reactive protein are major independent factors.
24:17
High levels mean much shorter survival than low
24:18
levels. Other tumor characteristics matter, too.
24:21
A very large tumor, say over 12 centimeters,
24:24
or a poor response to initial treatment, meaning
24:25
lots of viable tumor left after chemo, predict
24:28
worse survival. Are there tools to help estimate
24:29
survival? Yes. We use predictive models, like
24:32
the Bayesian Belief Network. These take clinical
24:35
data and calculate survival probabilities, often
24:38
at 3 months and 12 months. This is incredibly
24:41
helpful, particularly for surgical decisions.
24:43
If predicted survival is less than 3 months,
24:46
major surgery is generally off the table. The
24:48
focus shifts entirely to comfort care, often
24:50
hospice. If survival is predicted between 3 and
24:53
12 months, we might favor less invasive procedures
24:56
with quicker recovery. But if predicted survival
24:58
is over 12 months, we can consider more durable,
25:01
complex reconstructions aiming for longer -term
25:04
function. One study by Bauer found survival after
25:07
fixing a pathological fracture was often less
25:10
than six months, similar to just getting radiotherapy
25:12
for pain, highlighting how advanced the disease
25:14
often is by then. It's also true that a single
25:17
solitary metastasis generally carries a better
25:19
prognosis than multiple METs, sometimes even
25:22
allowing for treatment with curative intent.
25:24
That's a very practical way to use prognosis
25:26
in decision -making. And preventing those fractures
25:29
is such a key goal, what tools or scoring systems
25:32
do we actually use to predict the bone's mechanical
25:34
strength and fracture risk? And importantly,
25:37
how reliable are they in the real world? Preventing
25:39
pathological fractures is definitely a major
25:41
objective. The most widely used tool for long
25:44
bones is Mural Scoring System. It scores four
25:46
things. The site, upper limb, lower limb, or
25:49
the high -risk peritrochanteric hip region. The
25:52
pain, mild, moderate, or functional weight -bearing
25:54
pain. The lesion type, elastic, mixed, or lytic
25:59
being weaker. And the size related to the bone's
26:01
diameter, less than 13, 1323, or over 23 cortical
26:05
destruction. And how does the score translate
26:06
to risk? A total score of nine suggests a 33
26:09
% fracture risk. A score of 8 suggests 15%, and
26:13
7 or below is about 4%. Generally, a score of
26:16
8 or 9 often triggers a discussion about prophylactic
26:18
fixation surgery to prevent the fracture. However,
26:22
Muriel's score, while common, has significant
26:24
limitations. Its sensitivity is okay, maybe 80
26:27
-90%, but its specificity is often quite poor,
26:29
only 30 -35%. That means it can miss some high
26:32
-risk lesions, but more often it might overpredict
26:35
risk, potentially leading to surgery that wasn't
26:37
strictly necessary. It doesn't fully capture
26:39
the nuances of mechanical stress or overall bone
26:41
quality. So clinical signs are still important?
26:44
Absolutely paramount, often more important than
26:46
the score. Excessive pain, especially pain that
26:49
gets worse with weight bearing or comes on suddenly,
26:52
is a huge red flag for an impending fracture.
26:54
And a classic sign for an impending hip fracture
26:57
is seeing an evulsion of the lesser trochanter
26:59
on x -ray. That little piece of bone pulls off
27:02
because the underlying bone is so weak. We also
27:05
have to remember x -rays aren't sensitive enough
27:06
early on. You need significant bone loss to see
27:09
it. The patient's symptoms are key. There's a
27:12
newer and importantly more accurate method called
27:15
CT rigidity analysis, or CTRA. It uses CT scan
27:19
data to directly measure bone density and geometry
27:21
at the weakest point. It estimates the bone's
27:24
resistance to bending, twisting, and axial loading.
27:26
How does that compare? It compares the results
27:28
to normal bone data, matched for gender and size.
27:31
If the calculated rigidity is reduced by more
27:33
than 35%, that indicates a significant fracture
27:36
risk. Studies show CTRA has better sensitivity,
27:39
specificity, positive and negative predictive
27:41
value than Merrill's score. It's a more objective
27:44
and reliable tool, though it does need specialized
27:47
software and expertise to perform. Hashtag comprehensive
27:49
management strategies. It's so clear that managing
27:52
this is incredibly complex, needing careful coordination.
27:56
How do we structure the overall therapeutic approach?
27:59
And why is that multidisciplinary team, the MDT,
28:02
just so fundamental to getting the best outcomes,
28:05
especially when balancing survival and quality
28:07
of life? You've hit the absolute core principle.
28:11
Managing bone metastasis demands an interprofessional,
28:14
multidisciplinary approach. It's just too complex
28:16
for one specialist alone. The team usually involves
28:19
the orthopedic surgeon, often an orthopedic oncologist,
28:22
radiologists interpreting the scans, radiation
28:25
oncologists, medical oncologists managing the
28:28
systemic cancer treatment. But crucially, it
28:30
also includes pain management specialists, social
28:33
workers, and often hospice nurses, especially
28:35
thinking about the patient's whole journey and
28:37
quality of life. So what are the main goals of
28:39
this team? The overarching goals are really focused
28:41
on preserving the patient's quality of life,
28:44
controlling their pain effectively, minimizing
28:46
those skeletal related events, and achieving
28:49
local tumor control where we can. Every decision
28:52
weighs up multiple factors. How widespread is
28:54
the disease? What's the patient's overall fitness,
28:57
their performance status? What's the assessed
28:59
fracture risk? And what are the potential side
29:02
effects of any treatment we propose? The focus
29:05
has to be ensuring the patient has a decent quality
29:07
of life. Many are frail, many have a terminal
29:10
diagnosis. So we have to be careful to avoid
29:13
unnecessary tests of procedures that just add
29:16
burden. For many, comfort care or hospice becomes
29:19
the most appropriate and compassionate path,
29:21
especially given that the prognosis for widespread
29:23
bone mets is often limited historically four
29:26
to 12 months. Although, as we've touched on,
29:29
new systemic treatments are starting to push
29:30
that time frame out for some people, which brings
29:32
its own set of challenges for longer term management.
29:34
That collaborative approach sounds essential.
29:37
Let's break down the non -surgical options within
29:39
that MDT framework. What are the main medical
29:42
therapies and radiation techniques we use? How
29:45
do they fit into the strategy for pain relief
29:47
and controlling the disease? Non -surgical management
29:50
is a huge part of the picture, especially as
29:52
palliation and quality of life are often the
29:54
primary goals. Pain control analgesia is obviously
29:57
a major focus. We usually start with NSAIDs,
30:00
then titrate up or add narcotics like opioids
30:02
as needed to keep the patient comfortable. Glucocorticoids,
30:06
steroids can sometimes help with pain, maybe
30:08
by reducing swelling around the tumor, but their
30:11
use needs careful MDT discussion due to potential
30:13
side effects or impact on biopsy results. Bone
30:16
modifying agents are crucial. These are the osteoclast
30:19
inhibitors. They significantly reduce SREs and
30:22
help with bone pain, decreasing overall morbidity.
30:25
The two main classes are bisphosphonates like
30:27
pomidrinate, zolderonic acid, and dinosunab.
30:30
How they work differently. Bisphosphonates reduce
30:32
bone breakdown and associated hypercalcemia.
30:35
They cut SRE risk by about 30 -40%. A key potential
30:38
side effect is osteonecrosis of the jaw, so dental
30:41
checks are important. Some also have direct anti
30:44
-tumor effects. Dinosumab is a monoclonal antibody
30:47
targeting Aran -KL, that key signaling protein.
30:50
It's actually been shown to be superior to zoledronic
30:53
acid in preventing SREs. It directly blocks osteoclast
30:56
formation. A big advantage is it's given subcutaneously
31:00
and isn't cleared by the kidneys, making it a
31:02
good option for patients with kidney problems.
31:05
Radiation therapy, RT, is a cornerstone, especially
31:07
for paneliation. Local field radiation is standard
31:10
for painful spots. It reduces pain in 50 -80
31:13
% of patients, complete relief in maybe 30%.
31:15
We also use it after surgery sometimes to consolidate
31:18
healing. Studies show a single dose, like eight
31:20
gray, is often just as good for pain relief as
31:23
longer courses, say 30 gray and 10 fractions,
31:25
though the single dose might need repeating more
31:27
often. Are there more targeted radiation options?
31:29
Yes. Stereotactic Body Radiation Therapy, SBRT,
31:34
delivers a very high -focused dose while sparing
31:36
surrounding tissues. It might be used for specific
31:39
spinal meds, from tumors usually resistant to
31:41
standard radiation, or sometimes for oligometastatic
31:44
disease. For very widespread disease, hemi -body
31:47
irradiation, treating half the body, is an option,
31:49
but used less now. And then there's bone -targeted
31:52
radiopharmaceutical therapy. These are radioactive
31:55
drugs like Strontium -89 or Radium -223 that
31:58
specifically target bone, delivering radiation
32:00
diffusely. Good for widespread pain, especially
32:03
from plastic meds like in prostate or breast
32:05
cancer, or if other treatments fail. Systemic
32:08
chemotherapy, of course, plays a role if the
32:10
primary cancer is responsive. Shrinking the primary
32:13
and other meds can reduce overall disease burden
32:15
and help with pain indirectly. And finally, local
32:18
ablation techniques. These are for persistent
32:20
or recurrent pain after radiation. Things like
32:22
radiofrequency ablation, RFA, using heat, or
32:25
cryoablation using freezing. Focused ultrasound,
32:28
FUS, is newer. Cementoplasty injecting bone cement.
32:31
Often PMMA is vital, especially for pelvic lesions
32:33
or other lytic defects. It provides immediate
32:35
stability. relieving pain and improving function
32:38
in about 80 % of cases. And for very vascular
32:41
tumors like kidney or thyroid meds, preoperative
32:44
angiomyelization can block blood supply, reducing
32:46
bleeding during surgery and potentially enhancing
32:48
pain relief. That's a really comprehensive non
32:51
-surgical toolkit. Now, for us in orthopedics,
32:54
surgery is often critical, but the goals are
32:57
different from standard trauma surgery. What
33:00
are the main aims of surgery here? What principles
33:02
guide these operations? And how do the approaches
33:05
vary depending on which limb or part of the limb
33:08
is affected? Surgery is indeed a vital component,
33:11
and you're right, the mindset is different. The
33:13
main goals are quite clear. treat or ideally
33:16
prevent broken bones, relieve severe pain, reduce
33:19
reliance on heavy pain meds, restore skeletal
33:22
strength and stability, and ultimately help the
33:25
patient regain function and independence for
33:27
daily activities. A really key principle is that
33:30
prophylactic stabilization, fixing the bone before
33:32
it breaks, leads to significantly better outcomes
33:35
than operating after a fracture. Patients have
33:37
shorter hospital stays or more likely to go home,
33:40
get back to activity faster, have fewer complications,
33:43
and may even live longer because they avoid the
33:44
major physiological hit of a fracture. It allows
33:47
us to coordinate surgery better with their systemic
33:49
treatment, too. What are the core surgical principles,
33:51
then? First, that golden rule again, biopsy first.
33:54
Complete workup before surgery, especially for
33:57
pathological fractures. Know what you're treating.
33:59
Second, our fixation doesn't rely on bone healing.
34:02
These lesions rarely heal. So we use strong hardware
34:05
plates, rods, nails, screws, often combined with
34:08
bone cement, PMMA, for immediate stability and
34:11
strength. PMMA lets patients bear weight sooner
34:13
and approves pain relief by filling the defect.
34:16
Third, a general rule is to protect the entire
34:18
bone. If you fix just the lesion, it might fail
34:21
above or below due to disease progression. So
34:24
we often use long, intramedullary nails that
34:26
span the whole bone. Fourth, post -operative
34:29
radiation is recommended for almost all patients
34:31
starting two, three weeks after surgery, covering
34:33
a whole surgical field and implant. It helps
34:35
mop up any remaining microscopic disease, unless,
34:38
of course, the patient is very near end of life
34:40
or had previous radiation there. And finally,
34:43
for solitary lesions, if the patient's prognosis
34:45
allows, we might consider more aggressive surgery
34:47
like wide excision aiming for local cure, though
34:50
that's less common than palliative stabilization.
34:52
That framework makes a lot of sense. Now, the
34:54
limbs have very different anatomy. Can you walk
34:57
us through the tailored surgical strategies for
35:00
different areas, the pelvis, the lower limb,
35:02
the upper limb, and maybe touch on the spine?
35:04
Absolutely. The approach has to be adapted to
35:06
the specific site, the extent of bone loss, and
35:08
the patient's prognosis and functional needs.
35:11
Let's start with the pelvis. We often use the
35:13
Anakin classification zones 1, 2, and 3. Zones
35:16
1 and 3 are generally non -weight -bearing, but
35:18
zone 2, the acetopelomyscium area, is critical
35:21
for weight -bearing. Lesions here, or involving
35:24
adjacent zones, are problematic. Treatment might
35:26
range from curatage and cementing for contained
35:28
lesions to major reconstructions for large defects
35:31
using custom implants, saddle processes, or even
35:34
total hip replacements reinforced with pins and
35:36
cement the Harrington technique if bone stock
35:38
is poor. The goal is always to restore stability
35:41
for sitting and potentially walking. Moving to
35:44
the lower limb, the most common site, femur accounts
35:46
for 75%. Pain and ability to walk are the main
35:49
concerns. In the proximal femur, hip area, impending
35:53
or actual fractures almost never heal. The standard
35:55
treatment is usually a bipolar hemiarthroplasty,
35:58
replacing the ball part of the joint, often with
36:00
a long stem to bypass a lesion. If the socket,
36:03
as a tabulum, is also involved, then a total
36:05
hip replacement. For very large lesions here,
36:07
sometimes an endoprosthesis, replacing a whole
36:09
segment of bone, gives the best stability and
36:11
allows early weight -bearing. For the femoral
36:14
shaft, the best option is usually a load -sharing
36:16
intramedullary nail, locked in place, often with
36:19
cement augmentation to fill defects. It provides
36:22
strong internal support. Distal fever near the
36:25
knee lesions are tricky, often poor bone quality,
36:28
multiple fragments. For smaller lesions, maybe
36:30
plate fixation with cement. But for extensive
36:33
destruction, especially involving the joint,
36:35
a composite total knee replacement, essentially
36:37
a large tumor prosthesis might be needed. The
36:40
tibia, shin bone, is less common. Upper tibia
36:43
is managed similarly to distal femur cement.
36:45
Plates may be replacement. Tivial shaft usually
36:47
gets a metal rod. Distal tibia often plates and
36:50
screws with cement. The foot is very rare, less
36:52
than 1%. Usually from lung, kidney, colon. Treatment
36:56
is very individual radiation, orthotics, maybe
36:58
limited surgery, sometimes even amputation of
37:00
a toe for pain control. And the upper limb? The
37:03
upper limb accounts for maybe 20 % of cases,
37:05
half of those in the humerus. It's less mechanically
37:08
stressed than the leg, so sometimes humeral mets
37:10
can be managed non -operatively with just radiation
37:12
if retracture risk is low. But they can severely
37:15
impair function. For the upper humerus, large
37:18
tumors might need a prosthetic replacement of
37:20
the top part of the bone. These are complex ops
37:23
and function can be limited because the rotator
37:25
cuff often needs to be detached and reattached.
37:28
Humeral shaft tumors are usually best treated
37:30
with intermedullary rods, often with cement,
37:33
spanning the whole bone for stability. Plates
37:35
are an option, but left common for the shaft.
37:38
Near the elbow, flexible nails can work while
37:40
preserving the joint. If the tumor goes into
37:42
the joint, an elbow replacement might be needed.
37:45
Forearm and hand mets are rare. Lung, breast,
37:48
renal are common primaries, usually treated with
37:50
rods, plates, or bracing. And the scapula, shoulder
37:53
blade, depending on extent, might need partial
37:55
or total scapulaectomy. And briefly, the spine.
37:59
The spine is the most common site overall, but
38:01
surgery is actually less common than you might
38:03
think. Radiation is preferred if there's pain
38:06
but no nerve damage or major instability. Surgeries
38:10
mainly for neurological deficits like cord compression,
38:13
ongoing pain after RT, or instability. Minimally
38:16
invasive techniques like vertebroplasty, cement
38:18
injection, and kyphoplasty, balloon inflation,
38:21
then cement, are widely used now, often off -label,
38:25
at major centers to stabilize fractures and relieve
38:28
pain effectively in selected patients. That's
38:30
incredibly detailed, thank you. It really highlights
38:32
the bespoke nature of these surgeries. But with
38:35
such complex operations, often in patients who
38:37
are already quite unwell, what are the potential
38:40
computations? And how much does the patient's
38:42
overall health weigh into the decision to even
38:44
proceed with surgery? That's a critical consideration.
38:47
Surgical treatment for metastatic bone disease
38:49
is definitely complex, and it inherently carries
38:52
higher risks than routine orthopedic surgery.
38:55
This is largely because the patients themselves
38:57
are often less healthy. They might have multiple
38:59
other health issues, be weakened by cancer treatments,
39:02
may be immunocompromised, generally more frail.
39:05
So standard risks are magnified. Exactly. They're
39:08
at increased risk of common surgical complications,
39:10
which can be much more serious for them. Things
39:12
like persistent pain, significant bleeding during
39:16
or after surgery, infection, which is particularly
39:18
dangerous if they're immunocompromised and damage
39:20
to nearby nerves or blood vessels, potentially
39:23
causing numbness or even paralysis. Beyond those
39:27
immediate risks, there's always the chance of
39:29
the tumor recurring locally or the underlying
39:31
cancer progressing elsewhere. And tragically,
39:34
sometimes patients can die from surgical complications
39:36
or simply due to the rapid progression of their
39:38
advanced cancer. Given all these potential downsides,
39:41
the decision to operate is never taken lightly.
39:44
It absolutely has to be a very careful, very
39:47
informed cooperative discussion. It involves
39:49
the patient, their family, the surgeon, the oncologist,
39:52
the whole team. We have to meticulously weigh
39:54
the potential benefits, pain relief, improved
39:57
function, better quality of life against these
39:59
very real and significant risks. The final decision
40:02
must align with the patient's overall goals,
40:04
their wishes and their prognosis, focusing on
40:06
what truly matters most to them. Hashtag tag
40:09
tag enhancing health care team outcome. So pulling
40:11
it all together, then, what are the key principles
40:14
for really enhancing health care team outcomes
40:16
when managing metastatic bone disease, especially
40:19
thinking about the patient's quality of life
40:21
across their entire journey from the initial
40:23
diagnosis right through to end of life care?
40:26
To really optimize outcomes, the absolute bedrock
40:29
principle, as we've said throughout. is that
40:31
interprofessional, multidisciplinary approach.
40:34
It's got to be a team effort focused consistently
40:36
on preserving quality of life, controlling pain,
40:39
minimizing those SREs, and achieving local tumor
40:41
control where appropriate and feasible. It's
40:44
about pooling expertise for the patient's benefit.
40:47
When we devise that initial treatment plan, it's
40:49
critical to consider the whole picture, all those
40:52
holistic patient factors. How far has the disease
40:54
spread? What's their functional capacity, their
40:56
performance status? What's the real risk of fracture?
40:59
And what are the potential burdens and side effects
41:01
of different treatments? We're constantly balancing
41:04
aggressive intervention against purely palliative
41:06
goals, and that balance can shift as the patient's
41:08
condition changes or their priorities evolve.
41:11
Pain management is a continuous thread throughout,
41:13
starting with simpler analgesics, titrating up,
41:16
adding opioids, maybe using adjuvant drugs or
41:19
referring to pain specialists for nerve blocks
41:21
or other interventions. Keeping the patient comfortable
41:23
is paramount. And crucially, we always need to
41:26
practice compassionate care. Recognize that many
41:28
patients are frail. Many are facing the end of
41:31
their life. Unnecessary tests, burdens of procedures,
41:34
these should be avoided. The focus might need
41:37
to shift entirely towards maximizing comfort,
41:39
dignity, and quality time. That's where key support
41:42
roles become so important. Having a dedicated
41:45
pain specialist involved, a social worker to
41:47
help navigate practical and emotional challenges,
41:50
and ideally, hospice or palliative care nurses
41:53
integrated early on. They are all essential to
41:55
ensure the patient maintains the best possible
41:57
quality of life throughout their illness, providing
42:00
both medical and vital psychosocial support.
42:03
And while historically prognosis was often limited,
42:06
we do need to remember that for some patients,
42:08
thanks to better systemic therapies, we are looking
42:10
at longer timeframes now. So, while quality of
42:13
life remains central, planning for durable solutions
42:15
and longer -term function is becoming increasingly
42:18
relevant for a subset of these patients. Hashtags,
42:20
hashtags, outro, what? Okay, let's just try and
42:22
unpack all of that. What an incredibly insightful
42:25
deep dive into the very complex world of extremity,
42:30
skeletal, and metastasis. We've really covered
42:33
the whole spectrum, haven't we, from the, well,
42:35
the insidious ways it spreads and those awful
42:37
SREs through the complex diagnostic pathways
42:39
right up to the highly individual. but always
42:42
patient -focused treatment strategies. And what's
42:45
really striking, I think, for us as clinicians
42:47
is seeing how things are constantly evolving.
42:49
The advancements in both medical and surgical
42:51
approaches mean we genuinely have better options
42:54
now for pain control and for maintaining function
42:56
for longer. But as you stressed, it all comes
42:58
back to that collaborative, multidisciplinary
43:01
teamwork, tailoring everything to the individual
43:03
patient, their unique prognosis, their needs,
43:06
their goals. So what does this mean for you,
43:08
our listeners in the medical profession? I think
43:10
it really highlights just how vital it is to
43:12
understand these nuances. It allows for more
43:14
precise interventions, more realistic conversations
43:16
with patients, and ultimately, truly patient
43:18
-centered care. Because the goal always, at every
43:21
single stage, has got to be maximizing that precious
43:23
quality of life. And it does raise a really important
43:26
question. for the future. As our systemic therapies
43:29
get better and better, extending life for patients
43:31
with metastatic disease, sometimes turning it
43:34
into more of a chronic condition, how will we
43:37
in orthopedics need to adapt our management?
43:40
How do we provide even more durable, functionally
43:43
robust, and perhaps less burdensome solutions
43:45
for people living longer, sometimes for years,
43:48
with bone metastasis? That's a challenge, I think,
43:51
that will really shape our practice going forward.
43:53
If you found this deep dive valuable today, please
43:55
do take just a moment to rate and share it with
43:58
a colleague who you think might also benefit
44:00
from these insights.