June 16, 2025 • 18 mins
⚕️ FREE MSRA PODCAST – Venous Ulcer
🎧 A high-yield breakdown of this common leg ulcer – caused by venous hypertension, key for MSRA and clinical practice.
🧠 Key Learning Points
📌 Definition
• Venous ulcers are chronic, shallow wounds that develop due to poor venous return and increased venous pressure in the lower limbs, especially around the medial malleolus.
📌 Causes & Risk Factors
• Chronic venous insufficiency
• Varicose veins
• Deep vein thrombosis (DVT)
• Prolonged standing/sitting
• Obesity
• Older age
• Leg injury or trauma
• Pregnancy
• Family history
💡 Mnemonic: VOLD-FLIP
Varicose veins, Obesity, Long-standing/sitting, DVT, Family history, Low calf pump, Impaired mobility, Pregnancy
📌 Pathophysiology
• Incompetent venous valves → retrograde flow → chronic venous hypertension
• Capillary leakage of fibrinogen → fibrin cuffing
• Impaired oxygen diffusion → tissue hypoxia
• Inflammation + poor healing → skin breakdown → ulcer
📌 Symptoms
• Shallow, irregular ulcers (typically gaiter region)
• Mild discomfort or painless ulcer
• Surrounding signs: haemosiderin pigmentation, venous eczema, atrophie blanche, oedema, lipodermatosclerosis
• Often bilateral or recurrent
📌 Differential Diagnosis
• Arterial ulcer – painful, punched-out, weak pulses
• Neuropathic ulcer – painless, plantar foot
• Pressure ulcer – over bony prominences
• Malignancy (Marjolin’s ulcer) – non-healing, rolled edges
• Vasculitis or RA-related ulcers
📌 Diagnosis
• Clinical – typical site + surrounding signs
• Must assess ABPI (Ankle-Brachial Pressure Index)
<0.8: contraindicates compression
1.3: suggests calcified arteries (e.g. diabetes) → false reading
• Consider: venous Doppler, biopsy (non-healing), ulcer swabs (if infected), patch testing (dermatitis)
📌 Management
• Compression therapy – gold standard for healing and preventing recurrence
• Debridement and wound dressings (e.g. foam, hydrocolloids)
• Topical steroids – for venous eczema
• Antibiotics – only if signs of infection
• Pentoxifylline 400mg TDS – for refractory ulcers
• Lifestyle: leg elevation, mobility, skin care
• Long-term compression hosiery (Class 2 or 3) post-healing
• Referral to vascular if ABPI <0.8, suspected malignancy, poor healing, or unusual site
📌 Complications
• Local infection, cellulitis
• Pain, delayed healing
• Psychological impact
• Malignant transformation (Marjolin’s ulcer)
• High recurrence if compression not maintained
📌 Prognosis
• ~45% heal within 6 months in community
• ~70% heal with specialist care
• Recurrence in 26–70%, especially if ulcer >1 year or large
• Poor prognostic signs: chronicity, large size, arterial disease, poor compliance
📎 More MSRA Resources for Venous Ulcer
📝 Revision Notes: https://www.passthemsra.com/topic/venous-ulcer-revision-notes/
🧠 Flashcards: https://www.passthemsra.com/topic/venous-ulcer-flashcards/
💬 Accordion Q&A Notes: https://www.passthemsra.com/topic/venous-ulcer-accordion-qa-notes/
🚀 Rapid Quiz: https://www.passthemsra.com/topic/venous-ulcer-rapid-quiz/
🎓 Full Course: https://www.passthemsra.com/courses/dermatology-for-the-msra/
#MSRA #MSRARevision #MSRATextbook #MSRAQuiz #MSRAQu
Mark as Played
Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
(00:00):
Welcome to the Deep Dive, your focused guide for MSRA revision.
We're aiming this squarely at you today, concentrating on high
yield facts. Our topic Venous ulcers.
Exactly. Think of this as your power
revision session. We're going to pull out the
absolute core knowledge on venous ulcers, the what, why,
how to spot them, how to manage them, all structured to help you
(00:21):
lock it in for the exam. Perfect, let's get straight to
it then. What's the basic definition we
need to know? OK, so at its heart, a venous
ulcer is a chronic wound, usually on the lower leg, and
it's caused directly by venous insufficiency.
Basically, the veins aren't doing their job properly.
Pressure builds up. Right, that high venous
pressure. Exactly.
High venous pressure leads to tissue damage, and that's what
(00:42):
results in the ulcer. OK.
High pressure in the leg veins is the root cause.
Where do we typically see these ulcers and what do they, you
know, look like? You'll most commonly find them
in the Gator area, so around theankle, especially the medial
malleolus, the inner ankle bone,but they can be lateral too.
Appearance wise, they tend to beshallow, maybe a bit irregular
in shape, sometimes weepy or with a sort of granulating base.
(01:05):
And the ulcer itself? Painful.
Sometimes it can be relatively painless, though the surrounding
inflammation often causes discomfort.
But really you need to look at the surrounding skin.
That often tells the story. Ah, the associated sound.
You'll often see clear signs of chronic venous disease, things
like varicose veins themselves, venous eczema, that itchy, dry,
(01:28):
inflamed skin. Then there's hemiseterin
pigmentation that. Brownish staining.
That's the one caused by iron leaking from capillaries.
You might also see atrophy blanch, these small white
scarred patches and venous flarewhich are like little clusters
of tiny dilated veins. Plus oedema swelling is common
and sometimes the skin gets quite thick, even warty so.
(01:49):
It's a whole picture, not just the whole in the leg.
It almost sounds like faulty plumbing doesn't it?
Like if the one way valves in the leg veins are leaky, blood
pools, pressure builds up downstream near the skin,
stresses the tiny capillaries, they leak, cause damage, and
eventually the skin breaks down.That's a really good analogy
actually. Those faulty valves let blood
(02:10):
fall back down, especially when standing, hiking up.
The pressure massively in the lower leg veins and that
pressure gets transmitted right down to the skin capillaries.
OK. So that leads us nicely into the
why the aetiology, you mentionedthe valves.
Can you walk us through that mechanism and who's most at
risk? Right.
So the core. The problem is that venous
insufficiency, usually because the valves in the deep or
(02:33):
perforating veins aren't workingproperly, they're incompetent.
This lets blood flow backwards or retrograde.
Instead of up towards the heart.Exactly which causes chronic
venous hypertension? Persistently high pressure in
those veins. This high pressure forces fluid
and big molecules like fibrinogen.
Involved in clotting, right? Yeah, that one, it pushes
(02:54):
fibrinogen out of the capillaries into the surrounding
tissue. This forms the sort of fibrin
cuffs around the capillaries, trapping them and blocking flow.
That, plus the high pressure itself and the inflammation it
causes leads to impaired oxygen delivery to the tissues.
Tissue Hypoxia. So the skin is starved of
oxygen. Pretty much.
It gets inflamed, fragile, and doesn't take maybe just a small
(03:18):
knock to break down. And once that ulcer forms, the
poor oxygen supply and inflammation make healing
incredibly slow. Makes sense, Tissue needs
oxygen. So who are the people most
likely to end up with these valve problems or high venous
pressure? What are the key risk factors we
should flag? OK, several key ones to remember
for the MSRA. A big one is a history of DVT,
(03:39):
deep vein thrombosis, Because that can directly damage the
valves, right? Having varicose veins already is
a clear sign of underlying weakness.
Obesity is important. Increases pressure, older age as
veins and vows naturally weaken.Then there's prolonged standing
or sitting makes the calf pump work harder against gravity.
Leg injuries can sometimes damage veins or impair that
(04:00):
muscle pump. Pregnancy too, temporarily
raises venous pressure. And finally, family history.
There's often a genetic component.
That's a quite a few. Is there a good way to maybe
group those or remember them easily?
Yeah, you could try mnemonic, maybe something like VOLDFLIP.
VLDFLIP. OK, break that.
Down South, V for varicose veins, O for obesity, L for
(04:21):
older age, D for DVT history, then F for family history, L for
long periods of standing or sitting, I for impaired calf
bump. Could be from injury, obesity,
even pregnancy and P for pregnancy itself.
VOLDFLIP varicose veins, obesity, older age, DVT, family
history, long standing setting, impaired pump pregnancy.
(04:43):
Got it. That's useful.
So we've covered the causes, therisks.
Let's just quickly nail down thepath of Physiology again.
Sure. So the absolute root is chronic
venous hypertension from those incompetent valves.
High pressure. This leads straight to tissue
hypoxia. Not enough oxygen getting to the
skin. Which triggers inflammation?
Exactly, inflammation follows. Then, because of the pressure
(05:03):
and inflammation, fluid and proteins leak out into the
tissues, causing the oedema and those fibrin cuffs we mentioned.
This leakage further damages thetissue structure and creates a
really hostile environment for healing.
The skin gets fragile, breaks down easily, ulcer forms, and
then it struggles to heal. It's a vicious cycle, OK?
Pressure, hypoxia, inflammation,leakage, tissue damage, poor
(05:26):
healing ulcer. Got it.
Now, critically, not every ulceron the leg is venous, is it?
Absolutely not, and differentiating is key.
So if you see a leg ulcer, how do you know it's specifically a
Venous 1 and not something else?What are the main things to roll
out? Good question.
The main differentials are arterial ulcers, neuropathic
ulcers especially in people withdiabetes, and pressure ulcers.
(05:47):
But you also have to keep in mind less common things like
vasculitis, ulcers linked to conditions like rheumatoid
arthritis and importantly, malignancy.
Malignancy Yes, a chronic non healing ulcer can sometimes
undergo malignant change into a type of skin cancer called a
squamous cell carcinoma that's known as a Margulin's ulcer.
Always needs consideration if anulcer looks odd or just won't
(06:09):
heal. OK, so how do we tell them apart
based on features? We look for the contrasts.
Venous ulcers, typically shallowgaiter area, maybe not too
painful itself, but with all thesurrounding skin changes the
pigmentation, eczema, edoema. Arterial ulcers usually much
more painful, often deeper. Look punched out, maybe on toes
(06:29):
or pressure points, and crucially you'll find weak or
absent foot pulses. Because the arteries aren't
delivering enough blood. Precisely neuropathic ulcers
think diabetes, often painless because of nerve damage, usually
deep, typically on the sole of the foot or under pressure
points, and you might see thicken skin hyperkeratosis
around the edge. And the Margeland Ulter.
Look for changes in a chronic wound, maybe a rolled raised
(06:51):
hard edge. Any suspicion, you biopsy it.
Rheumatoid ulcers can be sharp, deep, well defined, sometimes in
the top of the foot or calf. OK, let's try a quick scenario
for the listeners. You see an elderly patient ulcer
on the front of their shin. They say it's really quite
painful. It looks deeper than usual and
you struggle to feel their foot pulses, venous or leaning
(07:12):
elsewhere. With that combination
significant pain, deeper ulcer, and crucially, those diminished
pulses, you'd be strongly suspicious of an arterial
component, if not a primary arterial ulcer.
It doesn't fit the classic venous picture well, right?
That difference is vital for management, isn't it?
Before we get to management, just quickly, How common are
(07:34):
venous ulcers? Epidemiology.
They're very common, especially in older populations.
Estimates suggest maybe 1 to 3% of people in the UK develop one
at some point. The number of people with one
right now, the point prevalence is about 3 per 1000 people
overall. But higher in the elderly.
Much higher jumps up significantly, maybe to around
20 per 1000 in people over 80. And it's worth remembering socio
(07:57):
economic factors might play a role in healing rates, possibly
due to access to care or compliance.
OK. Definitely something we'll see.
So let's summarise the clinical picture and diagnosis typical
presentation. You're looking for that patient
profile. Often older, maybe abuse.
Might mention late heaviness, aching, swelling that's worse at
the end of the day or after standing better with elevation.
(08:19):
History might include DVT, varicose veins, family history.
Examination shows the ulcer, typically Gator area, shallow,
irregular, maybe weeping, surrounded by those skin
changes, pigmentation, eczema, induration, maybe oedema.
And diagnosis is mainly clinical.
Primarily, yes, based on that characteristic history and the
examination findings, the ulcer itself plus the signs of venous
(08:41):
insufficiency and always checking the foot pulses is part
of that initial assessment to help rule out significant
arterial disease. OK, history and exam are key.
What about investigations? Are they always needed?
While diagnosis is often clinical, investigations are
crucial, especially one in particular before you start
treatment, which is the Ankle Brachial Pressure Index, or
ABPI, absolutely essential. Why is the ABPI so critical
(09:04):
here? Because the main treatment for
venous ulcers is compression therapy, and you cannot safely
apply strong compression if the arterial supply to the leg is
significantly reduced. The ABPI measures that arterial
flow by comparing ankle pressureto arm pressure.
OK, So what ABPI value is the warning signal?
A key cut off is 0.80. If the ABPI is less than 0.80,
(09:26):
it indicates significant peripheral arterial disease.
Applying high compression could be dangerous.
It could worsen ischemia, potentially leading to tissue
loss. So ABPI 0.8 generally means high
compression is contraindicated or needs extreme caution and
specialist input. Less than .8.
No high compression without specialist review.
Got it. Any other pitfalls with ABPI?
(09:47):
Yes, there's another important one, an ADPI above 1.3 higher.
Is bad too. It usually suggests the arteries
are calcified and rigid. Often seen in patients with
diabetes or advanced kidney disease, they don't compress
properly when taking the pressure, giving a falsely high
reading. So an ADPI 1.3 doesn't mean the
flow is great, it means the reading isn't reliable and might
(10:08):
be masking underlying arterial disease.
It warrants caution and probablyfurtherly, vascular assessment
before compression. OK, that's a really important
nuance. So quick check.
Patient has a typical looking venous ulcer but their ABPI
comes back at .6. What's the immediate implication
for management? ABPI 26 is well below .8 that
(10:28):
confirms significant peripheral arterial disease.
You would not proceed with standard high level compression
therapy. This patient needs urgent
referral to vascular specialist to assess the arterial supply
properly before any compression decisions are made.
Clear ABPI first always. What other tests might be done?
A venous Doppler ultrasound is often helpful.
It can directly visualise the veins and confirm reflux.
(10:49):
That backward flow showing valveincompetence.
You might measure the ulcer sizeregularly to track healing.
Swabs are only useful if you clinically suspect infection.
Looking for redness, warmth, increased pain, pus.
Not routine swabbing then. No, definitely not.
Colonisation is normal, you onlytreat infection.
Patch testing could be done if you suspect contact dermatitis
(11:11):
from dressings or creams causingthe surrounding eczema.
And a biopsy is important if theulcer looks atypical, is very
large, or fails to heal after, say, 12 weeks, primarily to rule
out malignancy that Margolin's ulcer.
Basic bloods like FBCESRCRP might be done if you're
considering other underlying causes.
OK, that makes sense. So we've diagnosed, we've done
(11:33):
our crucial ABPI, now the management, how do we actually
fix these things? Right, the goals are simple.
Heal the ulcer, ease the symptoms, and stop it coming
back. And the absolute cornerstone,
the number one treatment is compression therapy.
Back to compression. Always graduated compression,
usually with multi layer bandagesystems, initially counteracts
that high venous pressure, supports the veins, reduces
(11:55):
oedema and improves venous return.
It creates an environment where healing can actually happen.
Once healed or for prevention, compression stockings class 1-2
or three depending on the severity, are vital long term.
Compression first and foremost. What else is involved in
precorated care management? Good wound care is essential
under the compression. That means debridement, cleaning
(12:17):
away any dead tissue, Slough or pus as that hinders healing.
Then appropriate dressings. Things like hydrocolloids or
foam dressings that maintain a moist wound environment are
often good as they help the skincells migrate across the wound
bed. Keep it clean, keep it moist.
What about medications? Antibiotics, but only if there
are clear signs of infection. Systemic antibiotics like
(12:38):
flucloxacillin might be used then.
Definitely not for routine use on uninfected ulcers.
For chronic ulcers, ones that are really struggling to heal
after maybe six months despite good compression, there's
medication called pentoxifiline.Pentoxifiline.
Yes, it's thought to improve microcirculation.
The dose mentioned is 400 milligrammes 3 times a day,
usually for about 6 months. And importantly, it's prescribed
(13:00):
in addition to compression, not instead of it.
Also, for that venous eczema around the ulcer, topical
steroids are often needed. Any other things mentioned?
Maybe less evidence based. The source material might
mention things like aspirin as apossible adjunct but needing
more research. Therapeutic ultrasound has
limited evidence. More specialist things like
hyperbaric oxygen, specific sprays like granulox, venous
(13:23):
surgery to correct reflux in suitable patients, or skin
grafting for large defects exist, but that's usually
secondary care. OK.
And when should we be referring patients on to specialists like
the vascular team? Key times for referral include
if there's no improvement after about two weeks of good primary
care, if the patient has diabetes or significant arterial
disease that ABPI 0.8, if you suspect malignancy or another
(13:48):
calls like vasculitis, if the ulcers in an unusual place, if
surrounding dermatitis is reallybad and not responding to
steroids, or if they might be suitable for venous surgery or
grafting. Basically, any concern or lack
of expected progress warrants specialist input.
Right. So clear pathways exist.
Wrapping up management, compression is gang, wound care,
(14:09):
pintoxa, filing for stubborn cases alongside compression,
treat infection, manage eczema. So what's the outlook, the
prognosis? It's quite variable, honestly.
It depends heavily on the ulcer size, how long it's been there,
the patient's overall health, comorbidities, and crucially,
their adherence to the treatment, especially the
compression. Healing can take weeks, but
often it takes months. And recurrence.
(14:30):
That's the big challenge. While many ulcers can be healed
with good care, the risk of themcoming back is high if the
underlying venous insufficiency isn't managed effectively long
term, primarily with lifelong compression.
How high is that risk? Figures vary, but the source
suggests maybe 45% heal by 6 months in the community, perhaps
70% with specialist care. But then 12 month recurrence
(14:52):
rates going to be anywhere from say 26% up to nearly 70%.
It's often a relapsing conditionfor many people.
Wow, that high? Are there factors that predict a
worse outcome? Poor prognostic signs.
Yes, definitely. Things like the ulcer having
been present for more than a year, that carries a very high
recurrence risk. Over 70% larger initial wound
(15:13):
size. A history of previous varicose
vein surgery. Ironically, an ABPI less than
.8, indicating mixed disease. Poor calf muscle pump function
if more than half the wound baseis covered in fibrin.
Lower socioeconomic status can be a factor and, perhaps
unsurprisingly, poor compliance with compression therapy.
OK, so chronic large ulcers, arterial involvement, and not
(15:33):
sticking with the compression are all bad signs.
What about other complications besides recurrence?
Well, infection is a major one, both local infection in the
ulcer and spreading infection like Cellulitis.
Delayed healing itself is a complication, sometimes leading
to massive wounds. Chronic pain can be significant.
There's a huge impact on qualityof life, mobility issues,
(15:53):
discomfort, psychological distress, social isolation, and
as mentioned that small risk of malignant change in very long
standing ulcers. So given all that, prevention
seems absolutely critical. How do we stop these starting
and how do we stop them coming back?
Absolutely. Primary prevention is about
stopping that first ulcer. It focuses on managing venous
insufficiency early, so encouraging mobility, leg
(16:17):
elevation when resting, avoidingleg injuries, wearing supportive
well fitting shoes, using emollients regularly to keep
skin healthy but avoiding potential sensitizers if eczema
is present. Lifestyle is key to weight
management, healthy diet, stopping smoking and for those
with early signs like varicose veins or ankle swelling,
starting compression hosiery early can prevent progression to
(16:38):
ulceration. OK, that's stopping the first
one. What about stopping at recurring
after it's healed? Secondary Prevention.
This is crucial because of that high recurrence rate.
The single most important thing is consistent long term wear of
correctly fitted compression hosiery, often recommended for
at least five years after healing, but realistically for
many patients it needs to be lifelong.
(16:59):
Managing comorbidities effectively, like diabetes or
heart failure is also important,and in some selected patients,
referral for consideration of venous surgery to correct the
underlying reflex might be appropriate.
So, final check for everyone listening after a venous ulcer
has healed, what is the absolutecornerstone of preventing
recurrence? Without a doubt, it's the
(17:19):
consistent long term use of correctly fitted compression
hosiery that's the key message for secondary prevention.
Perfect. That really sums it up.
We've covered a lot of ground there, the underlying pressure
problem, the valve failure, how it damages tissue,
differentiating from other ulcers, the crucial role of
ABPI, the management cornerstoneof compression, plus adjuncts
like pentoxophylline, the trickyprognosis and high recurrence
(17:43):
complications, and those vital prevention strategies.
Hopefully that focused review helps consolidate the key facts
for your MSRA prep. Definitely understanding that
pathophysiology, why compressionworks and how to spot the red
flags like low ABPI or atypical features.
Those are really high yield areas.
Absolutely. For more free MSRA revision
resources, do visit freem-sra.com.
(18:04):
And for the full premium revision cool kit, you can head
over to pass them sra.com. Thanks for joining us for this
deep dive. Best of luck with the revision.
Welcome to the Deep Dive, your focused guide for MSRA revision.
We're aiming this squarely at you today, concentrating on high
yield facts. Our topic Venous ulcers.
Exactly. Think of this as your power
revision session. We're going to pull out the
absolute core knowledge on venous ulcers, the what, why,
how to spot them, how to manage them, all structured to help you
(00:21):
lock it in for the exam. Perfect, let's get straight to
it then. What's the basic definition we
need to know? OK, so at its heart, a venous
ulcer is a chronic wound, usually on the lower leg, and
it's caused directly by venous insufficiency.
Basically, the veins aren't doing their job properly.
Pressure builds up. Right, that high venous
pressure. Exactly.
High venous pressure leads to tissue damage, and that's what
(00:42):
results in the ulcer. OK.
High pressure in the leg veins is the root cause.
Where do we typically see these ulcers and what do they, you
know, look like? You'll most commonly find them
in the Gator area, so around theankle, especially the medial
malleolus, the inner ankle bone,but they can be lateral too.
Appearance wise, they tend to beshallow, maybe a bit irregular
in shape, sometimes weepy or with a sort of granulating base.
(01:05):
And the ulcer itself? Painful.
Sometimes it can be relatively painless, though the surrounding
inflammation often causes discomfort.
But really you need to look at the surrounding skin.
That often tells the story. Ah, the associated sound.
You'll often see clear signs of chronic venous disease, things
like varicose veins themselves, venous eczema, that itchy, dry,
(01:28):
inflamed skin. Then there's hemiseterin
pigmentation that. Brownish staining.
That's the one caused by iron leaking from capillaries.
You might also see atrophy blanch, these small white
scarred patches and venous flarewhich are like little clusters
of tiny dilated veins. Plus oedema swelling is common
and sometimes the skin gets quite thick, even warty so.
(01:49):
It's a whole picture, not just the whole in the leg.
It almost sounds like faulty plumbing doesn't it?
Like if the one way valves in the leg veins are leaky, blood
pools, pressure builds up downstream near the skin,
stresses the tiny capillaries, they leak, cause damage, and
eventually the skin breaks down.That's a really good analogy
actually. Those faulty valves let blood
(02:10):
fall back down, especially when standing, hiking up.
The pressure massively in the lower leg veins and that
pressure gets transmitted right down to the skin capillaries.
OK. So that leads us nicely into the
why the aetiology, you mentionedthe valves.
Can you walk us through that mechanism and who's most at
risk? Right.
So the core. The problem is that venous
insufficiency, usually because the valves in the deep or
(02:33):
perforating veins aren't workingproperly, they're incompetent.
This lets blood flow backwards or retrograde.
Instead of up towards the heart.Exactly which causes chronic
venous hypertension? Persistently high pressure in
those veins. This high pressure forces fluid
and big molecules like fibrinogen.
Involved in clotting, right? Yeah, that one, it pushes
(02:54):
fibrinogen out of the capillaries into the surrounding
tissue. This forms the sort of fibrin
cuffs around the capillaries, trapping them and blocking flow.
That, plus the high pressure itself and the inflammation it
causes leads to impaired oxygen delivery to the tissues.
Tissue Hypoxia. So the skin is starved of
oxygen. Pretty much.
It gets inflamed, fragile, and doesn't take maybe just a small
(03:18):
knock to break down. And once that ulcer forms, the
poor oxygen supply and inflammation make healing
incredibly slow. Makes sense, Tissue needs
oxygen. So who are the people most
likely to end up with these valve problems or high venous
pressure? What are the key risk factors we
should flag? OK, several key ones to remember
for the MSRA. A big one is a history of DVT,
(03:39):
deep vein thrombosis, Because that can directly damage the
valves, right? Having varicose veins already is
a clear sign of underlying weakness.
Obesity is important. Increases pressure, older age as
veins and vows naturally weaken.Then there's prolonged standing
or sitting makes the calf pump work harder against gravity.
Leg injuries can sometimes damage veins or impair that
(04:00):
muscle pump. Pregnancy too, temporarily
raises venous pressure. And finally, family history.
There's often a genetic component.
That's a quite a few. Is there a good way to maybe
group those or remember them easily?
Yeah, you could try mnemonic, maybe something like VOLDFLIP.
VLDFLIP. OK, break that.
Down South, V for varicose veins, O for obesity, L for
(04:21):
older age, D for DVT history, then F for family history, L for
long periods of standing or sitting, I for impaired calf
bump. Could be from injury, obesity,
even pregnancy and P for pregnancy itself.
VOLDFLIP varicose veins, obesity, older age, DVT, family
history, long standing setting, impaired pump pregnancy.
(04:43):
Got it. That's useful.
So we've covered the causes, therisks.
Let's just quickly nail down thepath of Physiology again.
Sure. So the absolute root is chronic
venous hypertension from those incompetent valves.
High pressure. This leads straight to tissue
hypoxia. Not enough oxygen getting to the
skin. Which triggers inflammation?
Exactly, inflammation follows. Then, because of the pressure
(05:03):
and inflammation, fluid and proteins leak out into the
tissues, causing the oedema and those fibrin cuffs we mentioned.
This leakage further damages thetissue structure and creates a
really hostile environment for healing.
The skin gets fragile, breaks down easily, ulcer forms, and
then it struggles to heal. It's a vicious cycle, OK?
Pressure, hypoxia, inflammation,leakage, tissue damage, poor
(05:26):
healing ulcer. Got it.
Now, critically, not every ulceron the leg is venous, is it?
Absolutely not, and differentiating is key.
So if you see a leg ulcer, how do you know it's specifically a
Venous 1 and not something else?What are the main things to roll
out? Good question.
The main differentials are arterial ulcers, neuropathic
ulcers especially in people withdiabetes, and pressure ulcers.
(05:47):
But you also have to keep in mind less common things like
vasculitis, ulcers linked to conditions like rheumatoid
arthritis and importantly, malignancy.
Malignancy Yes, a chronic non healing ulcer can sometimes
undergo malignant change into a type of skin cancer called a
squamous cell carcinoma that's known as a Margulin's ulcer.
Always needs consideration if anulcer looks odd or just won't
(06:09):
heal. OK, so how do we tell them apart
based on features? We look for the contrasts.
Venous ulcers, typically shallowgaiter area, maybe not too
painful itself, but with all thesurrounding skin changes the
pigmentation, eczema, edoema. Arterial ulcers usually much
more painful, often deeper. Look punched out, maybe on toes
(06:29):
or pressure points, and crucially you'll find weak or
absent foot pulses. Because the arteries aren't
delivering enough blood. Precisely neuropathic ulcers
think diabetes, often painless because of nerve damage, usually
deep, typically on the sole of the foot or under pressure
points, and you might see thicken skin hyperkeratosis
around the edge. And the Margeland Ulter.
Look for changes in a chronic wound, maybe a rolled raised
(06:51):
hard edge. Any suspicion, you biopsy it.
Rheumatoid ulcers can be sharp, deep, well defined, sometimes in
the top of the foot or calf. OK, let's try a quick scenario
for the listeners. You see an elderly patient ulcer
on the front of their shin. They say it's really quite
painful. It looks deeper than usual and
you struggle to feel their foot pulses, venous or leaning
(07:12):
elsewhere. With that combination
significant pain, deeper ulcer, and crucially, those diminished
pulses, you'd be strongly suspicious of an arterial
component, if not a primary arterial ulcer.
It doesn't fit the classic venous picture well, right?
That difference is vital for management, isn't it?
Before we get to management, just quickly, How common are
(07:34):
venous ulcers? Epidemiology.
They're very common, especially in older populations.
Estimates suggest maybe 1 to 3% of people in the UK develop one
at some point. The number of people with one
right now, the point prevalence is about 3 per 1000 people
overall. But higher in the elderly.
Much higher jumps up significantly, maybe to around
20 per 1000 in people over 80. And it's worth remembering socio
(07:57):
economic factors might play a role in healing rates, possibly
due to access to care or compliance.
OK. Definitely something we'll see.
So let's summarise the clinical picture and diagnosis typical
presentation. You're looking for that patient
profile. Often older, maybe abuse.
Might mention late heaviness, aching, swelling that's worse at
the end of the day or after standing better with elevation.
(08:19):
History might include DVT, varicose veins, family history.
Examination shows the ulcer, typically Gator area, shallow,
irregular, maybe weeping, surrounded by those skin
changes, pigmentation, eczema, induration, maybe oedema.
And diagnosis is mainly clinical.
Primarily, yes, based on that characteristic history and the
examination findings, the ulcer itself plus the signs of venous
(08:41):
insufficiency and always checking the foot pulses is part
of that initial assessment to help rule out significant
arterial disease. OK, history and exam are key.
What about investigations? Are they always needed?
While diagnosis is often clinical, investigations are
crucial, especially one in particular before you start
treatment, which is the Ankle Brachial Pressure Index, or
ABPI, absolutely essential. Why is the ABPI so critical
(09:04):
here? Because the main treatment for
venous ulcers is compression therapy, and you cannot safely
apply strong compression if the arterial supply to the leg is
significantly reduced. The ABPI measures that arterial
flow by comparing ankle pressureto arm pressure.
OK, So what ABPI value is the warning signal?
A key cut off is 0.80. If the ABPI is less than 0.80,
(09:26):
it indicates significant peripheral arterial disease.
Applying high compression could be dangerous.
It could worsen ischemia, potentially leading to tissue
loss. So ABPI 0.8 generally means high
compression is contraindicated or needs extreme caution and
specialist input. Less than .8.
No high compression without specialist review.
Got it. Any other pitfalls with ABPI?
(09:47):
Yes, there's another important one, an ADPI above 1.3 higher.
Is bad too. It usually suggests the arteries
are calcified and rigid. Often seen in patients with
diabetes or advanced kidney disease, they don't compress
properly when taking the pressure, giving a falsely high
reading. So an ADPI 1.3 doesn't mean the
flow is great, it means the reading isn't reliable and might
(10:08):
be masking underlying arterial disease.
It warrants caution and probablyfurtherly, vascular assessment
before compression. OK, that's a really important
nuance. So quick check.
Patient has a typical looking venous ulcer but their ABPI
comes back at .6. What's the immediate implication
for management? ABPI 26 is well below .8 that
(10:28):
confirms significant peripheral arterial disease.
You would not proceed with standard high level compression
therapy. This patient needs urgent
referral to vascular specialist to assess the arterial supply
properly before any compression decisions are made.
Clear ABPI first always. What other tests might be done?
A venous Doppler ultrasound is often helpful.
It can directly visualise the veins and confirm reflux.
(10:49):
That backward flow showing valveincompetence.
You might measure the ulcer sizeregularly to track healing.
Swabs are only useful if you clinically suspect infection.
Looking for redness, warmth, increased pain, pus.
Not routine swabbing then. No, definitely not.
Colonisation is normal, you onlytreat infection.
Patch testing could be done if you suspect contact dermatitis
(11:11):
from dressings or creams causingthe surrounding eczema.
And a biopsy is important if theulcer looks atypical, is very
large, or fails to heal after, say, 12 weeks, primarily to rule
out malignancy that Margolin's ulcer.
Basic bloods like FBCESRCRP might be done if you're
considering other underlying causes.
OK, that makes sense. So we've diagnosed, we've done
(11:33):
our crucial ABPI, now the management, how do we actually
fix these things? Right, the goals are simple.
Heal the ulcer, ease the symptoms, and stop it coming
back. And the absolute cornerstone,
the number one treatment is compression therapy.
Back to compression. Always graduated compression,
usually with multi layer bandagesystems, initially counteracts
that high venous pressure, supports the veins, reduces
(11:55):
oedema and improves venous return.
It creates an environment where healing can actually happen.
Once healed or for prevention, compression stockings class 1-2
or three depending on the severity, are vital long term.
Compression first and foremost. What else is involved in
precorated care management? Good wound care is essential
under the compression. That means debridement, cleaning
(12:17):
away any dead tissue, Slough or pus as that hinders healing.
Then appropriate dressings. Things like hydrocolloids or
foam dressings that maintain a moist wound environment are
often good as they help the skincells migrate across the wound
bed. Keep it clean, keep it moist.
What about medications? Antibiotics, but only if there
are clear signs of infection. Systemic antibiotics like
(12:38):
flucloxacillin might be used then.
Definitely not for routine use on uninfected ulcers.
For chronic ulcers, ones that are really struggling to heal
after maybe six months despite good compression, there's
medication called pentoxifiline.Pentoxifiline.
Yes, it's thought to improve microcirculation.
The dose mentioned is 400 milligrammes 3 times a day,
usually for about 6 months. And importantly, it's prescribed
(13:00):
in addition to compression, not instead of it.
Also, for that venous eczema around the ulcer, topical
steroids are often needed. Any other things mentioned?
Maybe less evidence based. The source material might
mention things like aspirin as apossible adjunct but needing
more research. Therapeutic ultrasound has
limited evidence. More specialist things like
hyperbaric oxygen, specific sprays like granulox, venous
(13:23):
surgery to correct reflux in suitable patients, or skin
grafting for large defects exist, but that's usually
secondary care. OK.
And when should we be referring patients on to specialists like
the vascular team? Key times for referral include
if there's no improvement after about two weeks of good primary
care, if the patient has diabetes or significant arterial
disease that ABPI 0.8, if you suspect malignancy or another
(13:48):
calls like vasculitis, if the ulcers in an unusual place, if
surrounding dermatitis is reallybad and not responding to
steroids, or if they might be suitable for venous surgery or
grafting. Basically, any concern or lack
of expected progress warrants specialist input.
Right. So clear pathways exist.
Wrapping up management, compression is gang, wound care,
(14:09):
pintoxa, filing for stubborn cases alongside compression,
treat infection, manage eczema. So what's the outlook, the
prognosis? It's quite variable, honestly.
It depends heavily on the ulcer size, how long it's been there,
the patient's overall health, comorbidities, and crucially,
their adherence to the treatment, especially the
compression. Healing can take weeks, but
often it takes months. And recurrence.
(14:30):
That's the big challenge. While many ulcers can be healed
with good care, the risk of themcoming back is high if the
underlying venous insufficiency isn't managed effectively long
term, primarily with lifelong compression.
How high is that risk? Figures vary, but the source
suggests maybe 45% heal by 6 months in the community, perhaps
70% with specialist care. But then 12 month recurrence
(14:52):
rates going to be anywhere from say 26% up to nearly 70%.
It's often a relapsing conditionfor many people.
Wow, that high? Are there factors that predict a
worse outcome? Poor prognostic signs.
Yes, definitely. Things like the ulcer having
been present for more than a year, that carries a very high
recurrence risk. Over 70% larger initial wound
(15:13):
size. A history of previous varicose
vein surgery. Ironically, an ABPI less than
.8, indicating mixed disease. Poor calf muscle pump function
if more than half the wound baseis covered in fibrin.
Lower socioeconomic status can be a factor and, perhaps
unsurprisingly, poor compliance with compression therapy.
OK, so chronic large ulcers, arterial involvement, and not
(15:33):
sticking with the compression are all bad signs.
What about other complications besides recurrence?
Well, infection is a major one, both local infection in the
ulcer and spreading infection like Cellulitis.
Delayed healing itself is a complication, sometimes leading
to massive wounds. Chronic pain can be significant.
There's a huge impact on qualityof life, mobility issues,
(15:53):
discomfort, psychological distress, social isolation, and
as mentioned that small risk of malignant change in very long
standing ulcers. So given all that, prevention
seems absolutely critical. How do we stop these starting
and how do we stop them coming back?
Absolutely. Primary prevention is about
stopping that first ulcer. It focuses on managing venous
insufficiency early, so encouraging mobility, leg
(16:17):
elevation when resting, avoidingleg injuries, wearing supportive
well fitting shoes, using emollients regularly to keep
skin healthy but avoiding potential sensitizers if eczema
is present. Lifestyle is key to weight
management, healthy diet, stopping smoking and for those
with early signs like varicose veins or ankle swelling,
starting compression hosiery early can prevent progression to
(16:38):
ulceration. OK, that's stopping the first
one. What about stopping at recurring
after it's healed? Secondary Prevention.
This is crucial because of that high recurrence rate.
The single most important thing is consistent long term wear of
correctly fitted compression hosiery, often recommended for
at least five years after healing, but realistically for
many patients it needs to be lifelong.
(16:59):
Managing comorbidities effectively, like diabetes or
heart failure is also important,and in some selected patients,
referral for consideration of venous surgery to correct the
underlying reflex might be appropriate.
So, final check for everyone listening after a venous ulcer
has healed, what is the absolutecornerstone of preventing
recurrence? Without a doubt, it's the
(17:19):
consistent long term use of correctly fitted compression
hosiery that's the key message for secondary prevention.
Perfect. That really sums it up.
We've covered a lot of ground there, the underlying pressure
problem, the valve failure, how it damages tissue,
differentiating from other ulcers, the crucial role of
ABPI, the management cornerstoneof compression, plus adjuncts
like pentoxophylline, the trickyprognosis and high recurrence
(17:43):
complications, and those vital prevention strategies.
Hopefully that focused review helps consolidate the key facts
for your MSRA prep. Definitely understanding that
pathophysiology, why compressionworks and how to spot the red
flags like low ABPI or atypical features.
Those are really high yield areas.
Absolutely. For more free MSRA revision
resources, do visit freem-sra.com.
(18:04):
And for the full premium revision cool kit, you can head
over to pass them sra.com. Thanks for joining us for this
deep dive. Best of luck with the revision.
Popular Podcasts
On Purpose with Jay Shetty
I’m Jay Shetty host of On Purpose the worlds #1 Mental Health podcast and I’m so grateful you found us. I started this podcast 5 years ago to invite you into conversations and workshops that are designed to help make you happier, healthier and more healed. I believe that when you (yes you) feel seen, heard and understood you’re able to deal with relationship struggles, work challenges and life’s ups and downs with more ease and grace. I interview experts, celebrities, thought leaders and athletes so that we can grow our mindset, build better habits and uncover a side of them we’ve never seen before. New episodes every Monday and Friday. Your support means the world to me and I don’t take it for granted — click the follow button and leave a review to help us spread the love with On Purpose. I can’t wait for you to listen to your first or 500th episode!
Dateline NBC
Current and classic episodes, featuring compelling true-crime mysteries, powerful documentaries and in-depth investigations. Special Summer Offer: Exclusively on Apple Podcasts, try our Dateline Premium subscription completely free for one month! With Dateline Premium, you get every episode ad-free plus exclusive bonus content.
24/7 News: The Latest
The latest news in 4 minutes updated every hour, every day.