Transcription
Rah, the radiant sun god of Ancient Egyptians, revered as the creator of all things and the bringer of life. Without the sun, our planet would be but another dark rock floating in the void of space. But its rays give life through chlorophyll and photosynthesis to build fields of green to be grazed on by animals, culminating in that pinnacle of all human experiences: the Big Mac.
In this video, we'll be eating—oops, sorry—exploring what you need to know about actinic keratosis for Primary Care dermoscopy. And if you make it to the end of this video, I'll be sharing a link with you to the coolest 3-minute video using an ultraviolet camera that everyone under the age of 35 needs to see, called solar keratosis. But ditch the "solar" bit. Why? Because when abbreviated in patient notes, it becomes SK, which could be misconstrued as squamous cell carcinoma, and you get confused, as I used to, which isn't difficult. But make it easy for yourself at the start of your dumbass adventure: call these AK keratosis, or AKs for short.
What causes them? In a nutshell, this—no, no, no, not a woman smiling at you semi-naked on a beach—white skin, no sun protection from the sun's ultraviolet light. You may be smiling now, lady, but give it time. Give it time. The problem is, the sun not only brings life, but it also brings skin damage and death through ultraviolet rays. I feel a diagram coming on.
To understand actinic keratosis, you need to understand ultraviolet radiation. UVC is screened out by the ozone. Fortunately, without it, you'll get severe sunburn within 5 minutes. Watch the Tom Hanks film called Finch to understand what the world would be like without an ozone layer. Crops would die, and humans, most life on Earth, would probably become extinct. That leaves us with UVA and UVB to contend with. I remember their effects like this: A is for aging. It degrades collagen and elastin in the dermis, resulting in more wrinkles, thinner, more even skin, vessels dilated with thinner walls, so much more easily damaged. B is for burning. Redness and pain, both cause DNA damage in the keratinocytes, the most common one being the gene that encodes the p53 suppressor protein, called the guardian of the genome. But it's not all bad news. UVB enables vital vitamin D production in the skin, and UVA produces tanning without the need for a sunbed. Just make sure you don't rely on clouds to save your skin. UVB is stopped by glass, but UVA isn't. Just look at this gentleman's face. What do you notice? If I told you he was a truck driver for 26 years, my question to you is this: which side of the truck was he sitting on?
The effects of UV photodamage on the skin is called dermathelioisis. Note, lentigines are another form of skin response to ultraviolet radiation that you will often see. An extreme example being this lady with multiple lentigines on her arms. Therefore, you often find lentigines and actinic keratosis on the same area of skin due to their common cause. And when the two collide, you get what's called a pigmented actinic keratosis.
Incidents and prevalence of AKs varies widely across continents. A survey in South Wales and mid-UK shows showed 24% of over 60s had at least one AK, with a linear increase from the ages of 60 onwards. And in Australia, 50% of white-skinned individuals over 40 have at least one.
How do you identify AKs and what can you see on dermoscopy? Their diagnosis is primarily clinical rather than dermoscopic, and we use a grading system from Olsen et al., which you can remember using this sentence: "Touch cornflakes and worry." Grade one actinic keratosis, I call "touch" because they're hardly visible, flat, pink macules, easier to feel and more difficult to see. The abnormal keratinocytes are located near the basement membrane and don't affect the full thickness of the epidermis. Sometimes mistaken for just a patch of dry skin. A trial with emollient will tell you if that's the case. I find dermoscopy most useful for these early actinic keratoses. Take this patch on this gentleman's cheek. It's been there a few months and not responded to over-the-counter emollient. Here's the dermoscope. Note the background erythema due to dermal vascular dilation. These are called rosettes in a four-leaf clover type shape. They are a type of shiny white structure that's best seen under polarized light dermoscopy. Many rosettes on top of the erythema gives the so-called strawberry pattern of early actinic keratosis. This pattern is most commonly seen on the face, head, and neck due to the flat dermoepidermal junction of the skin. An increase in skin adnexal openings. Note how the rosettes turn from their four-leaf clover shape to a round white ring as I switch between polarized and non-polarized light. Let's look at the dermoscopy of this lady's nose. Can you spot the background erythema, a bit of keratin scale, and rosettes? Smaller rosettes are mainly caused by polarized keratin material at the infundibular level in adnexal openings of the skin, and large rosettes mainly by concentric peripheral fibrosis.
Moving on to grade two actinic keratosis, which I call "cornflakes" because they often have adherent, moderately thick scales, just like a cornflake on the skin, set on an erythematous base. They are easily felt and seen. There's lots of grade one's as well. The stuck-on scales, keratin, much like a cornflake, which covers up the underlying epidermal changes, but surrounding this, you can see some rosettes. We call this field changes because there's a whole field of ultraviolet damaged skin and not just an isolated actinic lesion, and may include any or all of the grades of actinic keratosis from grades one to three.
With grade three actinic keratosis, it's time to start to worry. Why? Because these very thick hyperkeratotic lesions can be difficult to differentiate from early squamous cell carcinomas. The abnormal keratinocytes take up the full thickness of the epidermis, and if very dysplastic, a histopathologist might label them as "in situ." On dermoscopy, note what are called white structureless areas that are not expected in flat epidermal keratinizing lesions but are very common in SCCs. They correspond to significant acanthosis of highly keratinized cells, and if this is present, the lesion will not be flat. To make matters worse, recent studies demonstrate that this clinical grading does not accurately match with histological classification, with the Olsen grading being lower than the assumed histological grade in 62% of cases.
Why do actinic keratoses matter? AKs matter not just because of their cosmetic issues patients suffer, which is primarily their reason for attending, because they suggest that this has already happened and is at risk of this happening, if indeed it hasn't already happened already, kind of thing. A single AK can do one of three things: it can enter into spontaneous remission, and at one year, 55% regress, although one in three will recur after 3 years. They can remain stable without progressing. They can transform into an SCC. An individual AK has a one in a thousand per year risk of becoming an SCC. The figure to remember is if a patient has 7.7 AKs, they have a 10% risk of developing an SCC in the next 10 years. Now, I don't know about you, but I've never seen 7% of an AK, but you get the idea.
Look, I hear you scream, "How can I avoid missing an invasive SCC, which can metastasize and kill your patient, which isn't good?" Let's face it. Here are a few red flags for you: ulceration, they shouldn't be seen on an AK. Bleeding, likewise, shouldn't occur. Recent growth, sounds cancerous to me. An indurated lump, in other words, a palpable lump underneath that scale, is a concern. AKs can be occasionally a little bit irritating, but they should not be painful. And remember the first rule of primary care dermoscopy: of all my two-week cancer care pathway referrals, this is by far the main reason I refer, and it is not a cancer. They say, "Nah, it's just an AK. I'll freeze it." You, you know what? Sometimes they need to make that call, and not us in primary care. Just make sure.
Because what should we do when we diagnose an actinic keratosis or a field change of actinic keratosis? Explain that they should reduce their ultraviolet light exposure from here on in, and that it has value. Why? Because regular use of sunscreens has shown to prevent the development of actinic keratoses and possibly the longer-term risk of cancer. How do we recommend our patients reduce their ultraviolet exposure? Well, let me show you. You recommend they find shade between the hours of 11:00 a.m. and 3:00 p.m. peak UV levels. Slip on clothing, tightly woven, particularly on the limbs. Slap on a hat, wide-brimmed to cover those stick-out ears. Slop on cream, SPF 30-plus for adults. Put shades on the eyes, sunglasses reduce the amount of ultraviolet damage which also occurs to the eyes. The only difference between your patients and me is I look good in this. Do you know what the best sunscreen is? Andy, what a house. But just make sure you stay away from the windows. Now I know why the kids are always inside on the PlayStation. Clever kids.
For individual AKs, cryotherapy works really well. The longer the freeze, the better the remission rate. The relationship between the duration of freeze and the clearance rate was examined in a three-dose study with a 12-month duration follow-up. After cryotherapy, a duration of 5 seconds showed a 39% cure rate. 5 to 20 seconds, it went up to 69%. And more than 20 seconds, there was an 83% cure. On the scalp and the face, this treats the individual AKs, but it doesn't affect their overall cancer risk.
Imiquimod, 5-fluorouracil, or Efudex. I use a lot. Here's the lady I showed you earlier with grade 1 AK on her nose. Once daily 5-fluorouracil for 4 weeks. Inflammation at 3 weeks, and a month after stopping treatment, a nice smooth skin. Redness of the inflammation already fading, and a patient happy. A couple of things I always do before prescribing it: I show patients how things will get worse before they get better, bringing up images from the internet like this lady on the screen to show and discuss with them. Manage the patient expectations. An example from my patients is this gentleman with a non-healing grade 2 AK on his cheek. He wanted treatment, and we discussed it. And here's his pictures at week two and at week three that he sent me, and then four weeks after stopping treatment, as promised.
There's a link down below in the description about a really well-made, short 3-minute video entitled "How the Sun Sees You" using UV video. I watched it several times and I really enjoyed it. Oh, Amy, Carrie, and Phil, what's that? You don't like your name and you want to change it to instead? SCC training, primary care dermoscopy for every general practice.
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