February 3, 2025 • 20 mins
In this episode of Rash Decisions, hosts Dr George Moncrieff and Dr Roger Henderson delve into actinic keratoses (AKs), also known as solar keratoses. With expert insights, they discuss the nature of these common sun-induced lesions, their role as markers of both UV exposure and damage, along with practical approaches to diagnosis.
Key Takeaways:
- How to differentiate AKs from other keratotic lesions, including Bowen’s disease, keratoacanthoma and squamous cell carcinoma (SCC)
- The significance of clinical grading and the concept of "field cancerization"
- Practical tips for dermatoscopic evaluation and deciding when to refer patients.
Tune in to enhance your understanding of AKs and how the majority can be managed within primary care settings.
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The views expressed in this podcast are of Dr George Moncrieff and Dr Roger Henderson. Fontus Health has not influenced, participated, or been involved in the programme, materials, or delivery of educational content.
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
(00:08):
Hello, and welcome again to thisRash Decisions podcast, where
we look at skin-related issues,conditions and treatments in an
interesting and informed way.
I'm Dr Roger Henderson.
I'm a GP with a long-standinginterest in this area of health.
And I'm Dr George Moncrieff.
I was also a GP, though I'venow retired from my practice.
And I was the chair of theDermatology Council for England.
(00:32):
So today, George and I are going tobe talking about actinic keratoses,
sometimes called solar keratoses.
First of all, down to basics, George.
Why the two names?
And why do we both prefer to use theterm actinic keratosis in our practices?
(00:58):
Well, both solar and actinic essentiallymean, 'from the sun', actinic
strictly means, 'from radiation'.
So they're both saying they're sundamaged areas of keratotic skin.
But I like to shorten actinic keratosesto AK and if I was shortening solar
keratoses it would be SK but I just preferto keep SK for seborrhoeic keratoses.
(01:22):
So if I say SK, or Seb K, I'm thinkingseborrhoeic keratosis, and if I
say AK, it's quite clear, I'm justtalking about actinic keratoses.
Yep.
Are these actually premalignant?
Certainly, when I was a medical student,there was lots of chatter about, you
know, you've got to be wary about these.
In my experience, it's vanishinglyrare that these cause what I would
(01:45):
call significant long-term problems.
I couldn't agree more, and Ithink that I hear too many people
saying that they're treating thembecause they are premalignant and
it's a very interesting question.
There's no doubt that they are inducedby ultraviolet light as are other skin
(02:06):
cancers like squamous cell carcinoma.
That's the main causefor the keratotic series.
It's in fact, it's your lifetimecumulative exposure to sunlight that
seems to continually increase the risk.
So these of course occur onsun damaged skin, but I think
they're nothing more than that.
They're a marker of the amountof UV exposure you've had and the
(02:27):
amount of UV damage you've had.
And that's where you happen also toget your squamous cell carcinomas.
The work of Professor Robin Marksin Australia, who back in 1988,
showed the risk of a single actinickeratosis becoming a squamous
cell carcinoma in his study wasless than one in a thousand.
(02:49):
Wow.
That's 0.1%.
My personal view is that anSCC doesn't start off life as a
great big, hard keratotic nodule.
It starts off life lookinglike an actinic keratosis.
And within a few months, itdeclares its true identity.
It's changing, it's growing.
(03:09):
Whereas the AK remains anAK or often disappears.
And at the end of the day,what is the risk in an immune
competent adult from an SCC?
Unless it happens, unfortunately, tobe on your lip or your ear or a site of
radiation damage, or a scar, the riskof an SCC metastasising is less than 1%.
(03:34):
So you've got possibly a 0.1%of it being something that might
transform into an SCC, and I don'tbelieve that happens very often.
Then you've got a 1% risk ofit metastasising, and SCCs are
generally quite well behaved tumours.
They metastasise to their regional nodes.
They don't, like melanomas,have distant metastases.
(03:55):
And then the final question youneed to ask yourself is, does
treatment affect the outcome?
i.e.
if you treat an AK, do you reduce therisk of the patient developing an SCC?
There was a study that showed that,yes, it does during the next four years.
But at four years, the number ofSCCs are identical in the treated
(04:19):
group and the non-treated group.
So there's little argument fortreating AKs to prevent SCCs.
So I'm not concerned about that.
I hope that makes sense.
Yeah.
It does.
I've probably lost track of thenumber of, 85, 90-year-old men
coming in with AKs on their headslooking a little bit concerned.
And, we both agree at the endof the day that it's not that
(04:42):
that's, gonna carry them off.
Also we mustn't forget, Ithink it is worth mentioning,
natural resolution, of AKs.
You know, these can simply get better,without us doing anything at all.
Yep, about 24%, a quarter of them resolvewithout any treatment at all every year.
So, I think of them as very, very benigntumours, and I think so do secondary care.
(05:04):
They don't want us to be referring them.
They don't want to have ourpatients with these at all.
The only worry I have aboutthem is that they do share the
same gene mutations as SCCs.
Around about 50% of AKs havea p53 gene mutation, and I
think 66% of SCCs have that.
And that's a very important genethat essentially recognises a cell
(05:27):
that's been exposed to some damage.
And that gene makes a decisionwhether to put the cell into a resting
phase so that it can repair its DNA.
Or whether it needs to destroy thecell through a process of apoptosis.
So that's what the p53gene is there to do.
It's not just in the skin, it's allaround the body, having this role at
determining what should be the outcome ofa damaged cell or cell with damaged DNA.
(05:51):
But if the p53 gene itself is damaged,then it's unable to execute that function,
and a cell that really should havebeen destroyed is allowed to persist.
And p16 is in a similar sort of vein.
So these genes are present in AKs andthey are present in SCCs, but that
doesn't make them premalignant in my book.
(06:14):
Yeah, agreed.
Now, you touched on the phrase keratoticseries, just run me through what that is,
because I've got in my head, AKs, squamouscells, Bowen's, and maybe even acanthomas.
And I suppose we mustn't forgetkeratin horns because I actually saw
someone with one of those last week.
So, let's look at the keratotic series.
(06:36):
Just remind people what wemean when we talk about those.
Well, it's a spectrum of increasinglyabnormal and malignant lesions.
Right at the benign end of thespectrum, you have the grade one actinic
keratosis, which can then go throughto a grade three actinic keratosis.
I'll come onto those later.
(06:57):
There's a subtly differentresponse to ultraviolet light
that some people, demonstrate andprobably genetically determined.
It's called porokeratosis.
And I'll mention that as well.
When you've got full thickness dysplasiain the epidermis, not just in the basal
layers of the epidermis as you see inthe actinic keratosis, when you've got
(07:20):
full thickness and the metaplasia ismore severe, more mitotic activity, we
call that Bowen's disease or epidermalor intraepidermal carcinoma in situ.
It's an in situ cancer.
But the basement membrane that, dividesthe epidermis from the dermis is intact.
That's Bowen's disease.
(07:41):
Then as you mentioned, there'sthis extraordinary entity
called a keratoacanthoma, [a]very rapidly developing tumour.
Which, for our purposes, we shouldtreat as if it's an SCC, although it's a
very, very well-differentiated SCC, andthey have an extremely good reputation
and typically disappear spontaneously.
(08:02):
But nevertheless, we should still referthose through the two-week bureau.
Then through to the well-differentiatedsquamous cell carcinoma through to
the poorly differentiated carcinoma.
So it's a spectrum from AKthrough to poorly differentiated
squamous cell carcinoma.
I think aside from that, is wherethere's a sudden development of keratin
(08:23):
forming a keratotic horn and you can getthat on top of a viral wart or an AK.
A number of things can justsuddenly form a keratotic horn.
The important thing with a keratotichorn is to examine the base.
If it's simply just a little horn comingoff the skin of the epidermis, you can nip
that off with some scissors or whatever.
(08:45):
But if there's a fleshy base to it, itcould be a keratotic element of an SCC.
So the critical thing is to feel the base.
If it's raised and shoulderedand indurated, firm, then
it's keratin on top of an SCC.
But if it's simply just keratincoming off the skin, then it's
just keratin coming off the skin.
(09:06):
So in addition to all this, there'sthe concept of field cancerization, a
term described by Slaughter back in, Ithink, the 50s or 60s, with oral cancer.
So most cancers, which we can see andmanifest, in the surrounding tissue,
the tissue that's been exposed tothe same environmental and other
(09:26):
factors, demonstrates abnormal cells,which may not be clinically evident.
That's known as field cancerization.
So if you've got a bald scalp likemine, I've almost certainly got several
AKs on it, but there are areas ofmy scalp that currently look normal,
but were I to put some treatment onthere, I would declare those, um, that
(09:48):
there is actually dysplasia there,but it's not clinically manifested.
And so that concept is quite importantwhen you're coming onto treatment and
it's telling patients what to expect.
Hmm.
These are all driven by UV exposure.
So, when I'm looking at somebody todecide, do I think this lesion could
be concerning, I'm looking for otherevidence of sun damage, such as, mainly
(10:10):
the UVA driven changes like solarelastosis, but also wrinkling, pigmentary
clumping or even solar lentigos.
These are all on the backgroundof the area where the AKs and
other tumours are developing.
They're all on sun exposed skin.
[This] reminds me of one of ourprevious podcasts, which is a little,
(10:32):
mnemonic, which I'd forgotten, andI've been remembering ever since
with ultraviolet light, the Afor ageing and the B for burning.
It's a really good one, to remember.
Also in previous podcasts, we'vetalked about the clinical findings
of some skin problems and thosecan occasionally be quite tricky to
differentiate or, or complicated.
I have to say though, in practice,I find AKs to be absolutely one
(10:55):
of the simplest skin lesions, todiagnose, I suspect you do as well.
I always go straight off the bat tolook at, things like the head, neck,
forearms, hands, quite simply becausethese are the most common sun-exposed
areas, and so most prone to sun damageas the name suggests, but, and I don't
know if you would agree with this, inmy experience, I've rarely seen an AK
(11:19):
greater than about a centimetre across.
They tend to have a white, rough surface,and usually flat, although one of the
kickers here is if they've got loads ofscale on them, they can feel slightly
raised and thickened and that can, ifyou're not careful, have you scratching
your head thinking, just a minute,this doesn't look like a typical AK.
(11:40):
But you mentioned grading.
Well, first of all, wouldyou agree with what I've been
doing in clinic over the years?
And how do you tend to grade them whenyou're looking at someone with an AK?
I can completely agree with howyou're looking at them and agree that
they're rarely that size, are they?
They're usually quite small.
Yeah.
Grade 1 clinically is hard to see,in fact, it's much more easily felt.
(12:04):
So, if you run the hand over thearea of sun damaged skin, you can
just feel a roughness, you can feelthat sort of sandpapery feel to it.
So, grade 1 are more easily felt.
There might be slightly erythematouspatches, a little bit of fine
white scale, but that's about it.
Grade two, you're actually seeingthese, they're discrete lesions,
(12:24):
erythematous base and scaly.
Then the grade three, I agree, can bevery difficult to distinguish from an SCC.
Do you remember when I was talking aboutsuperficial BCCs, I said, stretch them and
you'll demonstrate that 'whipcord' edge.
Yes.
That slightly raised edge, whichis revealed by stretching them.
Well, I do the very opposite here,with the patient's permission, with
(12:45):
a grade three actinic keratosis,I give it a very gentle squeeze.
I'm squeezing it for two reasons.
One, I'm squeezing it to feel forinduration, thickening in the dermis.
But the other reason for doing itis, if the patient says, "Oh, that
feels a little tender", that wouldpoint towards the possibility there's
some perineural invasion of thetumour, so there's nerve involvement.
(13:07):
So, if I squeeze it and the patient says,"Oh I can feel that", I'm not giving it
a hard squeeze, just a gentle squeeze,then I'd be more anxious about it.
But a grade three often has quite a bit ofscale to it as you say, and sometimes that
scale is said to look like a cornflake.
I could do a whole talk on scale.
I think it's a fascinating topic.
But when I'm describing the scale of anactinic keratosis, it's cornflake-like.
(13:30):
Under the microscope, pathologists havea much more accurate, grading system.
And what they're determining thereis the degree of mitotic activity,
how many mitotic cells they can see.
And the depth of dysplasia.
So in grade one, it's really down atthe base of the membrane and grade two,
it's extending further up and so on.
So they have a grading system whichdoes equate to how severe it is, whereas
(13:55):
the clinical one, the link between howsevere it is in the grading system and
what that means is much more vague.
I suppose just for completeness sake, ifyou're talking about keratotic lesions, we
ought to just mention arsenical keratoses.
When I mention that, people oftenthink, "Gosh, I haven't got patients
poisoning each other with arsenic", butthere is arsenic in parts of the world.
(14:15):
For a brief while, I was working for theHigh Commission in Bangladesh, and in
the water system, in the rivers therein the North, there's a lot of arsenic,
and they develop arsenical keratoses.
One of the big differences is thatthese are often multiple, and they are
not exclusively on sun-exposed skin.
So if you see something thatlooks like an actinic keratosis on
(14:38):
sun-protected skin, you might justneed to be thinking in the back of
your mind, could we be dealing withsomething like an arsenical keratosis?
Interesting.
Now, I know you're an absolutelymassive dermatoscope fan.
There are some pretty characteristicAK findings if you're squinting
down your dermatoscope.
In your experience, what would yoube seeing when you're looking at
(14:58):
an AK with your dermatoscope then?
If I'm really honest, I don't thinkI use a dermatoscope to look at
my obvious, straightforward AKs.
Sure.
But where it really comes intoits own is with the flat pigmented
lesion on the face where the worryis differentiating a pigmented AK
(15:20):
from an early lentigo melanoma.
But I'll come on to that.
With a grade one, there's reallyvery little to see generally, you
might see some dilatation of thepapillary network, so you get a
sort of vascular pseudonetwork.
There are two main vascular networksin the skin, there's a reticular
one and there's a papillary onethat goes between the rete ridges.
(15:42):
That superficial one becomes dilated andso it forms this vascular pseudonetwork.
And you may just see a few fine, whitescales, and that's about it probably.
By the time you get up to grade two,generally, there's a flush in the skin.
There's some background erythema.
And the keratin that we're feelingis typically keratin around
(16:04):
the follicular openings, whichbecome widened by this keratin.
So you get wide and whitefollicular openings.
WWF is how I remember it.
These wide and white follicular openingsand some of them are very wide and others
are a lot less wide on this backgroundof erythema and that gives an appearance
(16:26):
very [much] like a strawberry wherethe white pips are the WWF and the pink
background or the pinky, red backgroundis that erythema I'm describing.
The perifollicular hyperkeratosisusefully reflects the four lights
on your dermatoscope producing anartefact, which we call a rosette,
'cause it's just these four lights.
(16:46):
And actually if you rotateyour dermatoscope, the white
dots of the artefact movearound with the dermatoscope.
All that's telling you is that there'skeratin, um, clumped in a small area.
So it's not pathognomonic for AKs,but when you see lots and lots of
rosettes, half a dozen or more, it'svery, very characteristic for an AK.
(17:08):
These are best seen with polarisingdermatoscopy, interestingly,
because that causes less scatter.
Because they are quite superficial.
If you want to see thingsin the epidermis, I normally
suggest using contact, becausethat focuses a bit higher.
Polarising penetrates a bit deeper.
But if you want to see rosettes, youneed to use your polarising mode.
But they're very usefulwhen they're multiple.
(17:30):
By the time you've got to gradethree, I'm afraid all you're
going to see is a plug of scale.
So you've got this structurelesswhite, yellow scale.
Interestingly, grade threesare usually solitary.
And of course, there, thedifferential is the SCC, a grade
one, well-differentiated SCC.
And clinically, I'll distinguish those.
You may actually see features of anSCC under the dermatoscope, large white
(17:54):
circles and things, much, much largerthan the wide and white follicular
openings that you see in an AK.
Yeah.
But on the face, trying to distinguisha pigmented AK from an early
lentigo melanoma is challenging.
Everybody finds that challenging.
I think what you need to do is thinkof a pigmented AK as being essentially
a collision lesion between an actinickeratosis and a solar lentigo.
(18:19):
So you see features of both.
So typically you're looking for thebackground erythema, the wide and white
follicular openings, the rosettes.
And then the pigment of a solarlentigo, which is epidermal, so it's
light tan coloured brown, usuallysharply demarcated with sometimes
(18:40):
a scalloped or watermark edge.
Not collecting as a ring of pigmentaround hair follicles, which is
what you see in a lentigo melanoma.
But that's a notoriously verytricky area of dermatoscopy.
Everybody finds flat pigmentedlesions on the face challenging.
Agreed.
But it does suggest that, dermatoscopyremains really key in primary care.
(19:03):
We come back to the point there,to all our healthcare professionals
listening, to go on a dermatoscopycourse, we'd thoroughly recommend, one.
I don't know how theycan manage to practise.
It must be terrifying, practisingwithout a dermatoscope.
Well, that's an enormous amountwe've covered, I think this has
been a really good one, George.
We do hope you found, this overviewabout AKs helpful, and if you have,
(19:27):
then please leave us a review.
We love making these, and yourfeedback coming in is really helpful
to us, not only to help keep usgoing, but also to tap in as to
what you want to know more about.
We'd also like to thank our sponsorAproDerm® for all their help in putting
these Rash Decisions podcasts together.
We couldn't have done it without them.
(19:48):
So until the next time,it's goodbye from George.
Goodbye.
And as always, it's goodbye from me.
Goodbye.
Hello, and welcome again to thisRash Decisions podcast, where
we look at skin-related issues,conditions and treatments in an
interesting and informed way.
I'm Dr Roger Henderson.
I'm a GP with a long-standinginterest in this area of health.
And I'm Dr George Moncrieff.
I was also a GP, though I'venow retired from my practice.
And I was the chair of theDermatology Council for England.
(00:32):
So today, George and I are going tobe talking about actinic keratoses,
sometimes called solar keratoses.
First of all, down to basics, George.
Why the two names?
And why do we both prefer to use theterm actinic keratosis in our practices?
(00:58):
Well, both solar and actinic essentiallymean, 'from the sun', actinic
strictly means, 'from radiation'.
So they're both saying they're sundamaged areas of keratotic skin.
But I like to shorten actinic keratosesto AK and if I was shortening solar
keratoses it would be SK but I just preferto keep SK for seborrhoeic keratoses.
(01:22):
So if I say SK, or Seb K, I'm thinkingseborrhoeic keratosis, and if I
say AK, it's quite clear, I'm justtalking about actinic keratoses.
Yep.
Are these actually premalignant?
Certainly, when I was a medical student,there was lots of chatter about, you
know, you've got to be wary about these.
In my experience, it's vanishinglyrare that these cause what I would
(01:45):
call significant long-term problems.
I couldn't agree more, and Ithink that I hear too many people
saying that they're treating thembecause they are premalignant and
it's a very interesting question.
There's no doubt that they are inducedby ultraviolet light as are other skin
(02:06):
cancers like squamous cell carcinoma.
That's the main causefor the keratotic series.
It's in fact, it's your lifetimecumulative exposure to sunlight that
seems to continually increase the risk.
So these of course occur onsun damaged skin, but I think
they're nothing more than that.
They're a marker of the amountof UV exposure you've had and the
(02:27):
amount of UV damage you've had.
And that's where you happen also toget your squamous cell carcinomas.
The work of Professor Robin Marksin Australia, who back in 1988,
showed the risk of a single actinickeratosis becoming a squamous
cell carcinoma in his study wasless than one in a thousand.
(02:49):
Wow.
That's 0.1%.
My personal view is that anSCC doesn't start off life as a
great big, hard keratotic nodule.
It starts off life lookinglike an actinic keratosis.
And within a few months, itdeclares its true identity.
It's changing, it's growing.
(03:09):
Whereas the AK remains anAK or often disappears.
And at the end of the day,what is the risk in an immune
competent adult from an SCC?
Unless it happens, unfortunately, tobe on your lip or your ear or a site of
radiation damage, or a scar, the riskof an SCC metastasising is less than 1%.
(03:34):
So you've got possibly a 0.1%of it being something that might
transform into an SCC, and I don'tbelieve that happens very often.
Then you've got a 1% risk ofit metastasising, and SCCs are
generally quite well behaved tumours.
They metastasise to their regional nodes.
They don't, like melanomas,have distant metastases.
(03:55):
And then the final question youneed to ask yourself is, does
treatment affect the outcome?
i.e.
if you treat an AK, do you reduce therisk of the patient developing an SCC?
There was a study that showed that,yes, it does during the next four years.
But at four years, the number ofSCCs are identical in the treated
(04:19):
group and the non-treated group.
So there's little argument fortreating AKs to prevent SCCs.
So I'm not concerned about that.
I hope that makes sense.
Yeah.
It does.
I've probably lost track of thenumber of, 85, 90-year-old men
coming in with AKs on their headslooking a little bit concerned.
And, we both agree at the endof the day that it's not that
(04:42):
that's, gonna carry them off.
Also we mustn't forget, Ithink it is worth mentioning,
natural resolution, of AKs.
You know, these can simply get better,without us doing anything at all.
Yep, about 24%, a quarter of them resolvewithout any treatment at all every year.
So, I think of them as very, very benigntumours, and I think so do secondary care.
(05:04):
They don't want us to be referring them.
They don't want to have ourpatients with these at all.
The only worry I have aboutthem is that they do share the
same gene mutations as SCCs.
Around about 50% of AKs havea p53 gene mutation, and I
think 66% of SCCs have that.
And that's a very important genethat essentially recognises a cell
(05:27):
that's been exposed to some damage.
And that gene makes a decisionwhether to put the cell into a resting
phase so that it can repair its DNA.
Or whether it needs to destroy thecell through a process of apoptosis.
So that's what the p53gene is there to do.
It's not just in the skin, it's allaround the body, having this role at
determining what should be the outcome ofa damaged cell or cell with damaged DNA.
(05:51):
But if the p53 gene itself is damaged,then it's unable to execute that function,
and a cell that really should havebeen destroyed is allowed to persist.
And p16 is in a similar sort of vein.
So these genes are present in AKs andthey are present in SCCs, but that
doesn't make them premalignant in my book.
(06:14):
Yeah, agreed.
Now, you touched on the phrase keratoticseries, just run me through what that is,
because I've got in my head, AKs, squamouscells, Bowen's, and maybe even acanthomas.
And I suppose we mustn't forgetkeratin horns because I actually saw
someone with one of those last week.
So, let's look at the keratotic series.
(06:36):
Just remind people what wemean when we talk about those.
Well, it's a spectrum of increasinglyabnormal and malignant lesions.
Right at the benign end of thespectrum, you have the grade one actinic
keratosis, which can then go throughto a grade three actinic keratosis.
I'll come onto those later.
(06:57):
There's a subtly differentresponse to ultraviolet light
that some people, demonstrate andprobably genetically determined.
It's called porokeratosis.
And I'll mention that as well.
When you've got full thickness dysplasiain the epidermis, not just in the basal
layers of the epidermis as you see inthe actinic keratosis, when you've got
(07:20):
full thickness and the metaplasia ismore severe, more mitotic activity, we
call that Bowen's disease or epidermalor intraepidermal carcinoma in situ.
It's an in situ cancer.
But the basement membrane that, dividesthe epidermis from the dermis is intact.
That's Bowen's disease.
(07:41):
Then as you mentioned, there'sthis extraordinary entity
called a keratoacanthoma, [a]very rapidly developing tumour.
Which, for our purposes, we shouldtreat as if it's an SCC, although it's a
very, very well-differentiated SCC, andthey have an extremely good reputation
and typically disappear spontaneously.
(08:02):
But nevertheless, we should still referthose through the two-week bureau.
Then through to the well-differentiatedsquamous cell carcinoma through to
the poorly differentiated carcinoma.
So it's a spectrum from AKthrough to poorly differentiated
squamous cell carcinoma.
I think aside from that, is wherethere's a sudden development of keratin
(08:23):
forming a keratotic horn and you can getthat on top of a viral wart or an AK.
A number of things can justsuddenly form a keratotic horn.
The important thing with a keratotichorn is to examine the base.
If it's simply just a little horn comingoff the skin of the epidermis, you can nip
that off with some scissors or whatever.
(08:45):
But if there's a fleshy base to it, itcould be a keratotic element of an SCC.
So the critical thing is to feel the base.
If it's raised and shoulderedand indurated, firm, then
it's keratin on top of an SCC.
But if it's simply just keratincoming off the skin, then it's
just keratin coming off the skin.
(09:06):
So in addition to all this, there'sthe concept of field cancerization, a
term described by Slaughter back in, Ithink, the 50s or 60s, with oral cancer.
So most cancers, which we can see andmanifest, in the surrounding tissue,
the tissue that's been exposed tothe same environmental and other
(09:26):
factors, demonstrates abnormal cells,which may not be clinically evident.
That's known as field cancerization.
So if you've got a bald scalp likemine, I've almost certainly got several
AKs on it, but there are areas ofmy scalp that currently look normal,
but were I to put some treatment onthere, I would declare those, um, that
(09:48):
there is actually dysplasia there,but it's not clinically manifested.
And so that concept is quite importantwhen you're coming onto treatment and
it's telling patients what to expect.
Hmm.
These are all driven by UV exposure.
So, when I'm looking at somebody todecide, do I think this lesion could
be concerning, I'm looking for otherevidence of sun damage, such as, mainly
(10:10):
the UVA driven changes like solarelastosis, but also wrinkling, pigmentary
clumping or even solar lentigos.
These are all on the backgroundof the area where the AKs and
other tumours are developing.
They're all on sun exposed skin.
[This] reminds me of one of ourprevious podcasts, which is a little,
(10:32):
mnemonic, which I'd forgotten, andI've been remembering ever since
with ultraviolet light, the Afor ageing and the B for burning.
It's a really good one, to remember.
Also in previous podcasts, we'vetalked about the clinical findings
of some skin problems and thosecan occasionally be quite tricky to
differentiate or, or complicated.
I have to say though, in practice,I find AKs to be absolutely one
(10:55):
of the simplest skin lesions, todiagnose, I suspect you do as well.
I always go straight off the bat tolook at, things like the head, neck,
forearms, hands, quite simply becausethese are the most common sun-exposed
areas, and so most prone to sun damageas the name suggests, but, and I don't
know if you would agree with this, inmy experience, I've rarely seen an AK
(11:19):
greater than about a centimetre across.
They tend to have a white, rough surface,and usually flat, although one of the
kickers here is if they've got loads ofscale on them, they can feel slightly
raised and thickened and that can, ifyou're not careful, have you scratching
your head thinking, just a minute,this doesn't look like a typical AK.
(11:40):
But you mentioned grading.
Well, first of all, wouldyou agree with what I've been
doing in clinic over the years?
And how do you tend to grade them whenyou're looking at someone with an AK?
I can completely agree with howyou're looking at them and agree that
they're rarely that size, are they?
They're usually quite small.
Yeah.
Grade 1 clinically is hard to see,in fact, it's much more easily felt.
(12:04):
So, if you run the hand over thearea of sun damaged skin, you can
just feel a roughness, you can feelthat sort of sandpapery feel to it.
So, grade 1 are more easily felt.
There might be slightly erythematouspatches, a little bit of fine
white scale, but that's about it.
Grade two, you're actually seeingthese, they're discrete lesions,
(12:24):
erythematous base and scaly.
Then the grade three, I agree, can bevery difficult to distinguish from an SCC.
Do you remember when I was talking aboutsuperficial BCCs, I said, stretch them and
you'll demonstrate that 'whipcord' edge.
Yes.
That slightly raised edge, whichis revealed by stretching them.
Well, I do the very opposite here,with the patient's permission, with
(12:45):
a grade three actinic keratosis,I give it a very gentle squeeze.
I'm squeezing it for two reasons.
One, I'm squeezing it to feel forinduration, thickening in the dermis.
But the other reason for doing itis, if the patient says, "Oh, that
feels a little tender", that wouldpoint towards the possibility there's
some perineural invasion of thetumour, so there's nerve involvement.
(13:07):
So, if I squeeze it and the patient says,"Oh I can feel that", I'm not giving it
a hard squeeze, just a gentle squeeze,then I'd be more anxious about it.
But a grade three often has quite a bit ofscale to it as you say, and sometimes that
scale is said to look like a cornflake.
I could do a whole talk on scale.
I think it's a fascinating topic.
But when I'm describing the scale of anactinic keratosis, it's cornflake-like.
(13:30):
Under the microscope, pathologists havea much more accurate, grading system.
And what they're determining thereis the degree of mitotic activity,
how many mitotic cells they can see.
And the depth of dysplasia.
So in grade one, it's really down atthe base of the membrane and grade two,
it's extending further up and so on.
So they have a grading system whichdoes equate to how severe it is, whereas
(13:55):
the clinical one, the link between howsevere it is in the grading system and
what that means is much more vague.
I suppose just for completeness sake, ifyou're talking about keratotic lesions, we
ought to just mention arsenical keratoses.
When I mention that, people oftenthink, "Gosh, I haven't got patients
poisoning each other with arsenic", butthere is arsenic in parts of the world.
(14:15):
For a brief while, I was working for theHigh Commission in Bangladesh, and in
the water system, in the rivers therein the North, there's a lot of arsenic,
and they develop arsenical keratoses.
One of the big differences is thatthese are often multiple, and they are
not exclusively on sun-exposed skin.
So if you see something thatlooks like an actinic keratosis on
(14:38):
sun-protected skin, you might justneed to be thinking in the back of
your mind, could we be dealing withsomething like an arsenical keratosis?
Interesting.
Now, I know you're an absolutelymassive dermatoscope fan.
There are some pretty characteristicAK findings if you're squinting
down your dermatoscope.
In your experience, what would yoube seeing when you're looking at
(14:58):
an AK with your dermatoscope then?
If I'm really honest, I don't thinkI use a dermatoscope to look at
my obvious, straightforward AKs.
Sure.
But where it really comes intoits own is with the flat pigmented
lesion on the face where the worryis differentiating a pigmented AK
(15:20):
from an early lentigo melanoma.
But I'll come on to that.
With a grade one, there's reallyvery little to see generally, you
might see some dilatation of thepapillary network, so you get a
sort of vascular pseudonetwork.
There are two main vascular networksin the skin, there's a reticular
one and there's a papillary onethat goes between the rete ridges.
(15:42):
That superficial one becomes dilated andso it forms this vascular pseudonetwork.
And you may just see a few fine, whitescales, and that's about it probably.
By the time you get up to grade two,generally, there's a flush in the skin.
There's some background erythema.
And the keratin that we're feelingis typically keratin around
(16:04):
the follicular openings, whichbecome widened by this keratin.
So you get wide and whitefollicular openings.
WWF is how I remember it.
These wide and white follicular openingsand some of them are very wide and others
are a lot less wide on this backgroundof erythema and that gives an appearance
(16:26):
very [much] like a strawberry wherethe white pips are the WWF and the pink
background or the pinky, red backgroundis that erythema I'm describing.
The perifollicular hyperkeratosisusefully reflects the four lights
on your dermatoscope producing anartefact, which we call a rosette,
'cause it's just these four lights.
(16:46):
And actually if you rotateyour dermatoscope, the white
dots of the artefact movearound with the dermatoscope.
All that's telling you is that there'skeratin, um, clumped in a small area.
So it's not pathognomonic for AKs,but when you see lots and lots of
rosettes, half a dozen or more, it'svery, very characteristic for an AK.
(17:08):
These are best seen with polarisingdermatoscopy, interestingly,
because that causes less scatter.
Because they are quite superficial.
If you want to see thingsin the epidermis, I normally
suggest using contact, becausethat focuses a bit higher.
Polarising penetrates a bit deeper.
But if you want to see rosettes, youneed to use your polarising mode.
But they're very usefulwhen they're multiple.
(17:30):
By the time you've got to gradethree, I'm afraid all you're
going to see is a plug of scale.
So you've got this structurelesswhite, yellow scale.
Interestingly, grade threesare usually solitary.
And of course, there, thedifferential is the SCC, a grade
one, well-differentiated SCC.
And clinically, I'll distinguish those.
You may actually see features of anSCC under the dermatoscope, large white
(17:54):
circles and things, much, much largerthan the wide and white follicular
openings that you see in an AK.
Yeah.
But on the face, trying to distinguisha pigmented AK from an early
lentigo melanoma is challenging.
Everybody finds that challenging.
I think what you need to do is thinkof a pigmented AK as being essentially
a collision lesion between an actinickeratosis and a solar lentigo.
(18:19):
So you see features of both.
So typically you're looking for thebackground erythema, the wide and white
follicular openings, the rosettes.
And then the pigment of a solarlentigo, which is epidermal, so it's
light tan coloured brown, usuallysharply demarcated with sometimes
(18:40):
a scalloped or watermark edge.
Not collecting as a ring of pigmentaround hair follicles, which is
what you see in a lentigo melanoma.
But that's a notoriously verytricky area of dermatoscopy.
Everybody finds flat pigmentedlesions on the face challenging.
Agreed.
But it does suggest that, dermatoscopyremains really key in primary care.
(19:03):
We come back to the point there,to all our healthcare professionals
listening, to go on a dermatoscopycourse, we'd thoroughly recommend, one.
I don't know how theycan manage to practise.
It must be terrifying, practisingwithout a dermatoscope.
Well, that's an enormous amountwe've covered, I think this has
been a really good one, George.
We do hope you found, this overviewabout AKs helpful, and if you have,
(19:27):
then please leave us a review.
We love making these, and yourfeedback coming in is really helpful
to us, not only to help keep usgoing, but also to tap in as to
what you want to know more about.
We'd also like to thank our sponsorAproDerm® for all their help in putting
these Rash Decisions podcasts together.
We couldn't have done it without them.
(19:48):
So until the next time,it's goodbye from George.
Goodbye.
And as always, it's goodbye from me.
Goodbye.
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