Latest / European Society for Vascular Surgery / All You Need To Know About Diabetic Heel Ulcer Management with G. Clerici - #ESVS2026

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All You Need To Know About Diabetic Heel Ulcer Management with G. Clerici - #ESVS2026 · European Society for Vascular Surgery

0:12
Welcome to the ESVS Podcasts, live from ESVS
0:17
2026 in Belgrade. I'm Justin Woolgar and joining
0:21
me today is diabetic foot and wound care specialist
0:24
Dr. Giacomo Clerici from Padua, Italy. In this
0:30
interview, we are going to discuss one of the
0:32
more challenging and difficult problems in diabetic
0:35
patients, how to manage heel ulcers. Dr. Clerici,
0:40
welcome to the ESVS podcasts. Thank you for this
0:45
invitation. Thank you for having me here today.
0:48
Now, I know you have just done a very interesting
0:51
presentation on this topic at the meeting this
0:53
afternoon. And for those who missed your presentation,
0:57
I would like to ask some specific questions and
1:00
share your expertise on the management of these
1:02
patients. First off, Why are diabetic heel ulcers
1:07
difficult to treat compared to, say, a forefoot
1:10
ulcer? The heel is a very particular anatomical
1:14
functional area. There is relatively little soft
1:18
tissue between the skin and the calcaneus and
1:20
once the ulcer becomes deep, bone involvement
1:23
can occur quite easily. In addition, the heel
1:27
has to withstand considerable pressure during
1:30
standing and walking, so effective offloading
1:33
can be particularly challenging. And from the
1:36
vascular point of view, heel perfusion is also
1:38
complex, and many of these patients have significant
1:42
peripheral arterial disease. And this is why
1:45
heel ulcers generally have a worse prognosis
1:47
than forefoot ulcers. Vascular surgeons, we are
1:53
interested to find out if a patient with a heel
1:56
ulcer has any evidence of peripheral vascular
1:58
disease. And if so, does it need treating? In
2:02
your experience, what proportion of these wounds
2:05
have a significant ischemic component? A very
2:09
significant proportion, actually. I would be
2:12
cautious about giving a single person size because
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it depends very much on the population you are
2:19
treating. In a tertiary diabetic center, the
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prevalence of peripheral arterial disease is
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obviously much higher than in a general diabetic
2:28
population. But clinically, I think the important
2:31
message is that the ischemia should always be
2:35
actively excluded. in patients with diabetes
2:38
and with a heel ulcer. So we should essentially
2:43
be on the lookout for peripheral vascular disease
2:47
and ischemia. In terms of assessing these patients,
2:51
the guidelines from a number of societies, including
2:53
the IWGDF, ESVS, SVS, etc., have all suggested
2:59
using a combination of Doppler examination, ABPIs,
3:03
and toe pressures. This can be quite labor intensive
3:06
if you're in a clinic, for example. Is there
3:10
any one test you would choose that would give
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you a good idea to the vascularity of a patient's
3:17
foot? Unfortunately, I don't think there is one
3:21
perfect test. This is particularly true in patients
3:25
with diabetes because medial arterial classification
3:27
can make the ankle pressure and ABI misleading.
3:32
I prefer to combine the clinical examination
3:34
with Doppler waveforms assessment and toe pressure
3:39
whenever possible. The waveform gives us important
3:43
hemodynamic information while toe pressure can
3:46
provide additional information about distal perfusion.
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Also, TCPO2 can be extremely useful. Perfusion
3:55
is not a number. It is a clinical condition.
3:57
Yes, no, absolutely. In my own experience and
4:02
practice in the UK, we don't have access to skin
4:05
perfusion measures such as TCPO2. You did mention
4:09
briefly that you have had some experience. Do
4:12
you find it quite useful? Absolutely, yes. And
4:16
not just for detecting the presence of critical
4:20
limb ischemia, chronically entreated limb ischemia,
4:23
but also for checking the patients after the
4:26
revascularization. We found, for example, and
4:29
we published a lot about the TCPO2 values. We
4:32
found that if you have a patient with TCPO2 of
4:37
40 or higher than 40, the risk of major amputation
4:40
is close to zero. But also between 30 and 40,
4:45
we are still 10 % of patients who undergo an
4:49
amputation. That's very useful to know. Let's
4:52
take a scenario of a patient. If you would imagine,
5:00
for instance, a typical... Type 2 diabetic patient
5:04
in their 70s, overweight, diabetes, not particularly
5:08
well -controlled, hypertensive, you know the
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picture, and has a, let's say, a four to five
5:15
centimetre heel ulcer with a dry black necrotic
5:17
eschar. The surrounding skin is, say, a bit erythematous.
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What would be your approach in dealing with this
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patient? My first question would be... Is this
5:29
simple dry necrosis or is there infection underneath
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it? The urethema makes me concerned. I would
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assess the patient systemically, look carefully
5:39
for cellulitis, fluctuans, drainage, malodour,
5:43
crepitus or other signs suggesting deep infection
5:46
and obtain laboratory investigation and appropriate
5:50
imaging when indicated. At the same time, I would
5:53
immediately assess perfusion. If this is truly
5:56
a stable, dry, non -infected eschar in a severely
6:00
ischemic foot, I would be very cautious about
6:03
aggressively removing it before understanding
6:06
whether the heel can heal. On the other hand,
6:10
if there is wet necrosis and abscess spreading
6:12
infection or systemic involvement, then infection
6:15
control becomes urgent and surgical drainage
6:18
or debridement cannot be delayed. So the key
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is to define infection, perfusion, and depth
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of the tissue involvement before deciding the
6:28
sequence of the treatment. Would you always consider
6:32
debridement first, followed by revascularization
6:34
or the reverse? And under what circumstances
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would you perhaps change your approach? Well,
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when I have a deep infection where I have, for
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example, gangrene, wet gangrene, gas gangrene,
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abscesses, necrotizing facilities, the first
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step is always drainage, is always the urgent
6:54
surgical approach. In this case, infection takes
6:58
priority over revascularization. Different is
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if you have an ischemic foot, is an ischemic
7:04
ulcer or an ischemic dry gangrene. If it's dry
7:08
with no infection, of course, first revascularization.
7:13
Not infrequently, we often find at operation
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that these patients have calcaneal osteomyelitis.
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How much of the calcaneum can be excised while
7:23
still preserving function? if wound healing can
7:26
be achieved? Well, this is a very important question
7:29
because the objective should not simply be to
7:32
preserve be to preserve the foot anatomically.
7:38
We have to preserve a functional foot. In selected
7:41
patients, quite extensive partial calcanectomy
7:44
can be performed while maintaining a potentially
7:47
functional limb. But there isn't a fixed percentage
7:51
of calcaneus that can safely be removed in every
7:54
patient. Bone preservation is important, but
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leaving infected bones simply to preserve anatomy
8:00
is not limb salvage. Let's assume that this patient's
8:05
heel ulcer and foot is salivable and we are thinking
8:08
of revascularization. More often than not, when
8:11
we perform a CTA, for example, we find the tibial
8:15
vessels are tubes of chalk. What is your preferred
8:18
imaging modality for these patients? This is
8:22
exactly where CTA can become problematic in patients
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with severe medial calcification, particularly
8:29
below the knee and below the ankle calcium. can
8:32
make interpretation of the lumen extremely difficult.
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Duplex ultrasound is very useful, particularly
8:39
in an experienced hand. But when I needed a precise
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anatomical roadmap for revascularization, especially
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in a complex diabetic food, digital subtraction
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and geography remains extremely important. It
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allows us to know. only to assess the tibial
8:57
vessels, but also the pedal circulation and importantly
9:00
for heel ulcers, the vessels supplying the heel.
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And of course, it has the advantage that diagnosis
9:07
and endovascular treatment can often be performed
9:11
during the same procedure. I'm going to ask you
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another question. What about MRA? Well, MRI is
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another option we have. MRI is important, for
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example, when you have to diagnose osteomyelitis.
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It's a very good tool because you can see the
9:30
change of the marrow edema. And, of course, in
9:35
terms of MRI in the use of vessel purpose, you
9:40
can have some problem with calcification as well.
9:43
Moving on to... revascularization in these patients?
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Simply put, when and how? Would you consider
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a revasc even if the absolute toe pressure measurement
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was greater than 30 millimeters of mercury? A
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toe pressure above 30 millimeters of mercury
10:00
should never be interpreted as a meaning that
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the patient automatically has had a great perfusion
10:06
for healing. Thresholds are useful for estimating
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probability, but they are not absolute biological
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boundaries. If I have a large heel ulcer that
10:17
is not healing poor Doppler waveforms, significant
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arterial disease on imaging, or other evidence
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suggesting inadequate tissue perfusion, I would
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still consider revascularization, even with a
10:31
top pressure above 30 mmHg. If you manage to
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consider revascularization, is inline flow to
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the foot sufficient or does it have to be angiosome
10:46
specific? If I can achieve a direct angiosome
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-related flow to the heel, I think that is desirable.
10:54
Of course, we are in the ideal world, but actually
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we are in the real world. The heel is predominantly
11:00
supplied through the branches related to the
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posterior tibial and peroneal arteries system.
11:06
So restoring direct perfusion to the affected
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territory makes physiological sense. However,
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real -life diabetic arterial disease is often
11:14
extremely complex. If direct angiosome revascularization
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is not technically possible, good in -line flow
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to the foot with an effective pedal collateral
11:24
network may still be sufficient to achieve healing.
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So I see the angiosome concept as an important
11:31
target, but not as an absolute rule. The objective
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is to maximize effective tissue perfusion at
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the wound. So effectively do what you can with
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what's available. Suppose we have the situation
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where we have a successful revascularization
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and the wound fails to progress. Are there any
11:50
other options available? Well, first of all,
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I would question whether the revascularization
11:56
is still successful. A technically successful
11:59
procedure does not necessarily mean that tissue
12:02
perfusion is adequate several weeks later. So
12:05
I would reassess the vascular situation. We have
12:07
a recortesis, for example. Then I go back to
12:10
the fundamentals, infection, residual osteomyelitis,
12:14
pressure, necrotic tissue, edema, nutritional
12:17
status, metabolic control, and wound management.
12:19
I would also ask whether the mechanical problem
12:22
has really been solved. Offloading is important.
12:25
If all these factors have been addressed, we
12:29
can consider advanced wound therapies and reconstructive
12:33
options in selected patients. But before adding
12:36
another technology, I always ask a very simple
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question. Why is this wound not healing? Advanced
12:43
therapy cannot compensate for persistent ischemia,
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uncontrolled infection or inadequate offloading.
12:51
What about the role of negative pressure dressings?
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Once you've managed to revascularize a large
13:00
wound or a heel ulcer, in your experience, which
13:03
wound management system works for you? Well,
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negative pressure wound therapy can be extremely
13:08
useful, particularly after adequate debris mount,
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when we have a clean wound with viable tissue
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and we want to promote granulation. and manage
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exudate. I use it frequently in appropriately
13:21
selected heel wounds, but negative pressure wound
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therapy is a tool, not a treatment for the underlying
13:28
disease. It can replace revascularization, infection
13:31
control, surgical debridement, or offloading.
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I don't think the most important question is
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which commercial system we use. The important
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issue is selecting the right wound at the right
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stage. For me, the sequence is fundamental. Control
13:45
of infection, restore perfusion when necessary,
13:49
remove non -viable tissue of loaded heel, and
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then use the wound management technology that
13:54
best supports healing. And so we have a lot of
13:57
new technologies. When and under what circumstances
14:02
would you think about reconstructive surgery,
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such as flap coverage of a heel ulcer? Well,
14:08
only after the fundamental problems have been
14:11
addressed, then reconstruction becomes an option
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when we have significantly soft tissue loss,
14:17
exposed bones, tendons or other structures that
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are unlikely to achieve durable coverage with
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conservative wound management alone. But reconstruction
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of the heel is particularly demanding because
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the tissue has to survive and ultimately tolerate
14:34
pressure. So the question is not simply whether
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we can close the wound. The question is, can
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we create durable functional coverage that will
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tolerate loading? That decision should ideally
14:49
be made within a multidisciplinary team involving
14:52
diabetic surgeons, vascular surgeons, and reconstructive
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surgeons. You mentioned offloading in one of
15:02
your answers to the questions. What would you
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recommend in how to best use offloading in patients
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with heel ulcers? Well, offloading is absolutely
15:15
fundamental. You can perform excellent revascularization
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and excellent surgery, but if the patient continues
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to apply repetitive pressure to the heel, the
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wound may still fail. During the acute phase,
15:28
particularly with a large or deep ulcer, we often
15:31
need very aggressive heel pressure relief, sometimes
15:34
including complete avoidance of heel loading.
15:36
The device has to be selected according to the
15:39
wound, the patient's mobility, balance, vascular
15:42
status, and risk of falls. And offloading doesn't
15:47
stop when the wound closes. After healing, the
15:50
patients need an appropriate long -term strategy
15:53
because recurrency is a major concern. So I would
15:57
say that offloading is not a necessary treatment.
16:00
It is a part of the treatment for the first day
16:03
until well behind wound closure. So I have a
16:08
couple of questions in one. At what point would
16:12
you decide that a patient's heel ulcer is too
16:15
far gone to even consider salvage and offer a
16:18
primary amputation? And when would you decide
16:22
that further efforts, such as reattempting further
16:25
revascularization, is just going to be futile?
16:28
So this is probably the most difficult decision
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we make, and I think we need to change the way
16:34
we define success. The endpoint should not be
16:36
limb salvage at any cost. The real endpoint is
16:40
functional limb salvage. If technically I can't
16:43
preserve a foot, but the patient will undergo
16:46
months of repeated surgery, persistent infection,
16:49
prolonged hospitalization. and you ultimately
16:52
end up with a painful, unstable, and non -functional
16:56
limb that is not necessarily a successful outcome.
17:01
I consider the extent of tissue destruction,
17:04
calcaneal involvement, possibility of control
17:06
infection, revascularization options, expected
17:10
function, the patient general condition, and
17:13
very important, the patient's own goals. Similarly,
17:16
repeated revascularization makes sense only if
17:20
there is a realistic possibility that improving
17:24
perfusion will change the clinical outcomes.
17:27
Sometimes a well -planned amputation with good
17:30
rehabilitation offers better functional outcomes
17:33
than endless attempts at salvage. I know during
17:38
your presentation that you did mention using
17:42
antibiotic -laden cement injected into the calcaneum.
17:47
And I think you did say it was... relatively
17:51
new concept. Are there any other things like
17:54
that on the horizon or new developments that
17:57
could change the way we manage diabetic heel
17:59
ulcers? I think the future will probably come
18:03
from several areas rather than from one revolutionary
18:06
treatment. First, we are becoming much better
18:09
at assessing tissue perfusion rather than simply
18:12
arterial patency. This may help us understand
18:15
whether our revascularization errors. actually
18:19
improve perfusion where the wound needs it. Second,
18:24
endovascular technology continues to expand our
18:27
ability to treat very distal disease, including
18:29
complex below -the -ankle circulation. Third,
18:32
we are improving our surgical approach to calcaneal
18:35
osteomyelitis with more conservative and targeted
18:38
bone resection and increasingly sophisticated
18:40
strategy for local management of infection. We
18:44
are also seeing advance in wound reconstruction,
18:47
biological therapies, and technologies for monitoring
18:50
wound progression. But perhaps the biggest development
18:53
is conceptual. We are moving away from teeth.
18:57
treating the artery, the infection, and the wound
18:59
as separated problems. The future is a truly
19:03
integrated, multidisciplinary approach in which
19:06
perfusion, infection, surgery, wound healing,
19:08
biomechanics, and function are considered together
19:12
from the beginning. And ultimately, our goal
19:15
should not simply be to close a heel ulcer. Our
19:19
goal is to give the patients a healed, stable,
19:22
and functional limb, functional foot. Dr. Clarecci,
19:26
that's about all we have time for. Many thanks
19:28
for agreeing to take part in this podcast and
19:31
sharing your experience with us. I hope you have
19:34
an enjoyable Congress at the ESVS 2026. Thank
19:37
you very much. Thank you indeed.