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34 JCN 2018, Vol 32, No 6 I n a culture that is often called ‘youth obsessed’, there is a great emphasis on how to improve the appearance of our skin (Helfrich et al, 2008). Chronologic skin aging however, is a natural, genetically determined process which occurs with age and can be classified into four categories; fine wrinkles/texture, lack of firmness of cutaneous tissues, vascular disorders and pigmentation changes (Farage et al, 2008; Flament et al 2013), as well as the development of benign growths, such as seborrhoeic keratoses and angiomas. Many of the skin changes commonly associated with aging are actually normal Recognising solar damage in the elderly molecular changes amplified by the result of sun exposure, seen as deep wrinkles, sallowness and pigmentation changes. These changes are often referred to as ‘photoaging’ and describe the effects of ultraviolet (UV) light on the skin. It has been said that the effects of sunlight on the skin account for up to 90% of the visible skin changes seen in older age (Farage et al, 2008). Changes in elderly skin are both cosmetically and medically important. Extrinsic factors, such as sunlight, pollution, nicotine, repetitive squinting or frowning, diet and sleep also influence the visible changes seen during the aging process. Aged skin is also more susceptible to dryness and therefore itching, infection and Sara Burr, community dermatology nurse specialist, Norfolk Community Health and Care NHS Trust Skin changes due to aging are important to distinguish from those that are due to solar/sun damage. Knowledge of the common changes in the skin as it ages will help clinicians diagnose and assessing other conditions. Before exploring such skin changes, causing changes that are observed as solar damage. This article highlights skin changes due to aging and solar damage and what actions need to be taken, if any, to manage them appropriately. KEYWORDS: Solar/sun damage Skin changes Elderly skin Sara Burr SOLAR SKIN DAMAGE INSIGHT... a JCN learning zone feature www.jcn.co.uk/learning-zone autoimmune disorders, vascular complications and cutaneous malignancy, and most people over 65 have at least one skin disorder, with many having two or more (Kligman and Koblenzer, 1997). Table 1 shows comparisons between normal aging and photoaging. In chronologically aged skin, the epidermis is atrophic with a flattening of the epidermal-dermal junction resulting in general thinness and frailty. The dermis also becomes thinner with fewer fibroblasts and collagen, leading to wrinkling. Photoaged skin, in contrast, has an accumulation of elastin-containing material just below the dermal-epidermal junction, which is known as solar elastosis, and the collagen becomes disorganised and can look thickened. EFFECT OF ULTRAVIOLET (UV) RADIATION The sun provides a natural source of UV radiation in our environment. The optical spectrum refers to the electromagnetic radiation, measured in nanometers, that reaches the earth’s surface and ranges from 290–4,000 nanometers (nm). This includes gamma rays, x rays, UV rays, visible light, infrared light, micro and radio waves (Elsner et al, 2007). UV radiation, a small segment of the spectrum, is divided into short wave UVC (200–280nm), middle wave UVB (280–320nm) and long wave UVA (320–400nm). Factors such as the earth’s atmosphere, water vapour, ozone, carbon dioxide, air pollution, latitude, altitude, season, time of Aged skin is more susceptible to dryness and therefore itching, infection and autoimmune disorders, vascular complications and cutaneous malignancy, and most people over 65 have at least one skin disorder...’ Woundcare People Ltd
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Page 1: Recognising solar damage in the elderly - JCN...Before exploring such skin changes, ... positioning of the body/skin to the sun. Which rays penetrate the skin ... following organ transplant

34 JCN 2018, Vol 32, No 6

In a culture that is often called ‘youth obsessed’, there is a great emphasis on how to

improve the appearance of our skin (Helfrich et al, 2008). Chronologic skin aging however, is a natural, genetically determined process which occurs with age and can be classified into four categories; fine wrinkles/texture, lack of firmness of cutaneous tissues, vascular disorders and pigmentation changes (Farage et al, 2008; Flament et al 2013), as well as the development of benign growths, such as seborrhoeic keratoses and angiomas. Many of the skin changes commonly associated with aging are actually normal

Recognising solar damage in the elderly

molecular changes amplified by the result of sun exposure, seen as deep wrinkles, sallowness and pigmentation changes. These changes are often referred to as ‘photoaging’ and describe the effects of ultraviolet (UV) light on the skin. It has been said that the effects of sunlight on the skin account for up to 90% of the visible skin changes seen in older age (Farage et al, 2008).

Changes in elderly skin are both cosmetically and medically important. Extrinsic factors, such as sunlight, pollution, nicotine, repetitive squinting or frowning, diet and sleep also influence the visible changes seen during the aging process. Aged skin is also more susceptible to dryness and therefore itching, infection and

Sara Burr, community dermatology nurse specialist, Norfolk Community Health and Care NHS Trust

Skin changes due to aging are important to distinguish from those that are due to solar/sun damage. Knowledge of the common changes in the skin as it ages will help clinicians diagnose and

assessing other conditions. Before exploring such skin changes,

causing changes that are observed as solar damage. This article highlights skin changes due to aging and solar damage and what actions need to be taken, if any, to manage them appropriately.

KEYWORDS: Solar/sun damage Skin changes Elderly skin

Sara Burr

SOLAR SKIN DAMAGE

INSIGHT...a JCN learning zone feature www.jcn.co.uk/learning-zone

autoimmune disorders, vascular complications and cutaneous malignancy, and most people over 65 have at least one skin disorder, with many having two or more (Kligman and Koblenzer, 1997). Table 1 shows comparisons between normal aging and photoaging.

In chronologically aged skin, the epidermis is atrophic with a flattening of the epidermal-dermal junction resulting in general thinness and frailty. The dermis also becomes thinner with fewer fibroblasts and collagen, leading to wrinkling. Photoaged skin, in contrast, has an accumulation of elastin-containing material just below the dermal-epidermal junction, which is known as solar elastosis, and the collagenbecomes disorganised and canlook thickened.

EFFECT OF ULTRAVIOLET (UV) RADIATION

The sun provides a natural source of UV radiation in our environment. The optical spectrum refers to the electromagnetic radiation, measured in nanometers, that reaches the earth’s surface and ranges from 290–4,000 nanometers (nm). This includes gamma rays, x rays, UV rays, visible light, infrared light, micro and radio waves (Elsner et al, 2007).

UV radiation, a small segment of the spectrum, is divided into short wave UVC (200–280nm), middle wave UVB (280–320nm) and long wave UVA (320–400nm). Factors such as the earth’s atmosphere, water vapour, ozone, carbon dioxide, air pollution, latitude, altitude, season, time of

‘Aged skin is more susceptible to dryness and therefore itching, infection and autoimmune disorders, vascular complications and cutaneous malignancy, and most people over 65 have at least one skin disorder...’

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JCN 2018, Vol 32, No 6 35

SOLAR SKIN DAMAGE

Table 1: Comparison of changes seen in chronological aging and photoaging skin

Chronological aging PhotoagingFine wrinkles Deep, coarse wrinkles

Laxity Mottled pigmentation

Benign skin growths Sallowness (pale yellow)

Decreased cell turnover Dryness

Reduced sebum (dry skin) Telangectasia (tiny broken blood vessels)

Laxity

Atrophy (degeneration)

Leathery appearance

Elastosis (accumulation of abnormal elastic tissue)

Actinic purpura (connective tissue damage and easy bruising)

Pre-malignant lesions

Horny layer

Biosphere

Light spectrum

Stratosphere

Epidermis

Dermis

Subcutaneous

InfraredUV-C

UV-C

UV-B

UV-B

UV-A

UV-ASkin

200Wavelength (nm) 290 320 400 800

Skin penetration of UV ray

Figure 1.Penetration of UV rays into the skin.

day and cloud cover all play a part in the way that the sun’s radiation is modified before reaching the skin. The effect of the radiation on the body will also vary depending on the surface angles and positioning of the body/skin to the sun. Which rays penetrate the skin is of great importance in relation to what physiological changes are then seen on the skin. Currently, UVC rays only come from artificial UV sources and hardly penetrate the epidermis. UVB rays reach through the epidermis to the superficial dermis, while UVA rays can reach the deep dermis (Figure 1) (Diffy et al, 1977).

Studies have shown that the body receives different amounts of sunlight according to different

anatomical sites (Diffey et al, 1977). For example, the highest dose of light is received on the crown of the head, the shoulders receive about 66% of the total dose, the hand 30–50%, the back 40–60%, the chest 25–70% and the calves about 25% (Diffey et al, 1997). The amount of light received on the face is dependent on bodily

activity. The forehead receives 20–65% of the value of the crown of the head, the cheeks 15–40%, the chin 20–35%, and the nape of the neck 20–35%.

The amount of damage to the skin as the UV is absorbed is dependent on the genetics of the individual, including skin type as well as the cumulative dose of UV over their lifetime. When assessing someone’s skin, it is important to ask about UV exposure over their life. Did they grow up overseas, or work outdoors, or were they posted abroad during the war? Additional exposure to UV rays through activities like outdoor work, recreational activity, use of sunbeds or phototherapy for skin condition management will add to the cumulative dose and, therefore, the damage received and probably seen. If someone has a suppressed immune system, through taking immune-suppressive drugs following organ transplant or receiving radiation treatment, it is important to recognise that this will also lead to an increased risk of skin cancer.

The main UV burden for those not working outdoors and living in Europe is exposure at weekends and holidays, which normally affects the backs of the hands, forearms and face. Virtually all Caucasian Western individuals with normal recreational practices will have subclinical signs of skin damage by the time they are 15 years old. Visible skin changes start to become discernible in exposed skin from the early 30s (Farage et al, 2008).

Sun exposure is essential, not only for mood and emotional wellbeing, but also physiologically in the synthesis of vitamin D. For the fair-skinned population, skin type I or II, the effect of the sun is more severe because the body’s natural defences are less efficient than in those with darker skins, type IV and V (Flament et al, 2013).

One question to ask older patients is what happens to their skin when they are in the sun.

‘One question to ask older patients is what happens to their skin when they are in the sun. This will help to identify how quickly their skin takes to burn in the sun, and if they like sun exposure or shy away from it.’

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36 JCN 2018, Vol 32, No 6

SOLAR SKIN DAMAGE

This will help to identify how quickly their skin takes to burn in the sun, and if they like sun exposure or shy away from it. Those people with darker skin types (V or VI) will still show some sun damage histologically, but in most cases this is clinically unapparent. When UV radiation is absorbed by skin molecules, they can generate harmful compounds called reactive oxygen species (ROS), which lead to damage to the cell walls, lipid membranes, mitochondria (structures within cells, which convert energy from food into structures that the cells can use) and DNA (Helfrich et al, 2008). Other chemical reactions, as a result of UV absorption, cause collagen breakdown, which, because collagen is the cornerstone of skin strength, eventually leads to visible wrinkles.

Repeated exposure to UV insults the skin and has an immunosuppressive effect inhibiting antigen presentation and stimulating the release of inflammatory cytokines. Cytokines are proteins in the skin that are stimulated by ultraviolet exposure and cause the visible changes that are seen on the skin and shown as images in this article (Deevya et al, 2010). The depth of UV ray penetration in the skin will determine what is seen externally and will vary according to UV ray and skin structures affected. Table 2 highlights these clinical findings, some of which are illustrated in the photographs.

EFFECTS OF CHRONIC UV EXPOSURE ON THE SKIN

Repeated UV radiation and injury on the skin leads to an accumulation of damage. In addition to the features seen in Table 2, the development of non-melanoma skin cancers is on the increase (Cancer Research, 2018a). Non-melanoma skin cancer (NMSC) is the most common group of cancers, accounting for roughly 20% of all new malignancies and 90% of all skin cancers registered in the UK and Ireland (Cancer Research, 2018a).W

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JCN 2018, Vol 32, No 6 37

SOLAR SKIN DAMAGE

Table 2: Types of skin damage

Structure Elderly skin Sun-damaged skin Epidermis Thin Keratosis — solar or chelitis, disseminated

superficial actinic porokeratosis

Dermis Thin, inelastic, wrinkled Yellowish — brown dotted or plaque-like thickening (solar elastosis), nodules on the pinna (ear rim)

Hypodermis Fold formation None

Blood vessels Cherry angiomas, venous lakes Diffuse telangiectasia, erythema (redness), brown pigmentation on side of neck, purpura

Melanocytes Solar lentigo, flat seborrhoiec keratoses

Mottled, irregular areas of hypopigmenation and hyperpigmentation, brown solar/actinic keratoses

Hair Gray, alopecia None

Sebaceous glands Senile sebaceous hyperplasia Solar comedones, nodular cutaneous elastoides

Eccrine glands Dry None

Nails Splitting into layers, linear striations None

The two major types of NMSC are basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). Basal cell carcinoma affects the basal cells at the bottom of the epidermis (outer section of skin) and represents about 74% of NMSCs. BCCs usually grow fairly slowly, over months or years, they rarely metastasise and almostnever cause death, but can erode local anatomical structures, especially on the head and neck if they are left untreated. They can present as nodular lesions, superficial or morphoeic. The presence of any non-healing lesion/spot/mark on a patient’s skin should be noted. Any patches identified as persisting or going and coming back in the same place should be assessed, particularly if they are on sun exposed sites (Cancer Research, 2018b).

INSIGHT...for individual e-learning and

CPD timeHaving read this article, why not go online and take your individual learning further by testing your knowledge of this topic in the INSIGHT section of the FREE JCN e-learning zone (www.jcn.co.uk/learning-zone)?

If you answer the accompanying online questions correctly, you can download a certificate to show that you have completed this JCN e-learning unit on recognising solar damage in the elderly.

Then, add the article and certificate to your free JCN revalidation e-portfolio, as evidence of your continued learning — safely, securely and all in one place: www.jcn.co.uk/revalidationW

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38 JCN 2018, Vol 32, No 6

SOLAR SKIN DAMAGE

Squamous cell carcinoma represents around 23% of NMSCs. It is a cancer of the cells producing keratin; a waxy substance that helps to form the protective outer layer of the epidermis. SCCs are much more aggressive, they can grow very quickly, even within weeks. They invade underlying structures and may metastasise and can cause death. NMSCs are rarely fatal, but due to their high incidence represent a significant burden to health services (National Cancer Registration and Analysis Service, 2018).

The most aggressive skin cancer is melanoma, comprising 4–5% of all skin malignant growths. The combined incidence for males and females has increased by 64% for men and 39% for women over the last decade (2003–2005 – 2013–2015) (Cancer Research UK, 2018b).

Most BCC, SCC and melanomas need surgically excising, so referral to secondary care is necessary. Superficial BCCs can be treated with specialised topical creams, however, these will usually be initiated within secondary care too.

Actinic keratoses are precursors of SCC so, although not dangerous per se, it is important that they are identified and managed to minimise this development. It is estimated that 23% of the population aged over 60 will have an actinic keratosis (Cancer Research, 2018a). The risk of this turning into SCC increases with length of duration and total number. The national Primary Care Dermatology Society guidelines (PCDS, 2018) explain the management of these depending on their presentation, which ranges from being pink and flat to being redder and with thick scale or a keratotic horn.

WHEN TO REFER

When assessing any patient for skin changes, it is of paramount importance that solar damage is noted. If the patient has any scars, especially on sun-exposed skin sites, it is always good to elicit their cause. Once a patient has had a

Squamous cell carcinoma with central ulceration

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KEY POINTS

The skin’s aging process is determined by genes and presents as fine wrinkles/ textures, lack of firmness, vascular disorders and changes in pigment.

The role of ultraviolet (UV)light on the skin can amplify the natural processes of change, which means wrinkles can appear deeper and pigmentation darker or lighter.

The effect of extrinsic factors, such as pollution, nicotine, diet or sleep can also influence the visible changes seen on the skin as it ages.

Sun exposure on the skin is essential for mood and emotional wellbeing, as well as synthesis of vitamin D.

Repeated exposure to UV light can have an immunosuppressive effect which stimulates inflammatory processes within the skin.

Accumulation of UV damage presents in different ways on the skin. Key features are of skin lesions never healing properly and being on sun exposed areas such as backs of hands, faces, necks and torsos for gentlemen.

Any persistently different skin changes should be report to a healthcare professional for assessment and referral on to a dermatologist if needed.

skin cancer, malignant or not, there is a risk of developing another (Cancer Research UK, 2018b), so it is crucial to remain vigilant for further skin changes. If any non-healing lesion is identified, it should be recorded in care plans with a referral made to GP, specialist community skin cancer or dermatology nurse for assessment. The patient may themselves know about such lesions, so always listen out for any insight. During any assessment, previous sun exposure should be discussed with lesions being recognised and documented to form a baseline against which to measure any change.

TREATMENT OF AGING SKIN AND WOUND CARE

It is never too late to prevent further aging of the skin. The goal of treatment should include prevention of further photoaging, especially burning. There are several ways this can be achieved: Sunscreen — these contain

both chemical and physical filters which interfere with the reactions in the skin which occur with UV exposure. There is much evidence around the effectiveness of sunscreens to reduce photoaging (Elsner et al, 2007), and the use of a sun protection factor cream of at least 15 with a UVA filter, on a daily basis, between April and September in the Northern hemisphere, is recommended. People with a risk of vitamin D deficiency should have their levels checked and supplements given if needed

Avoidance of UV radiation from artificial sources, and between 11.00am and 3.00pm in the summer months

Use of sun protective clothing, such as long sleeves and wide-brimmed hats, as well as UV absorbing sunglasses while out in the sun.

CONCLUSION This article has highlighted the normal processes of skin aging and how exposure to UV light amplifies these, and what can present later

in life as UV radiation accumulates. Community nurses should have an understanding of how to help patients prevent further solar damage, and know when particular skin lesions need to be assessed for further treatment.

REFERENCES

Cancer Research UK (2018a) Online data. Available online: www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/skin-cancer/incidence#heading-Two

Cancer Research UK (2018b) Online data. Available online: www.cancerresearchuk.org/about-cancer/skin-cancer/living-with/skin-care-after-skin-cancer

Deevya L, Narayanan MPH, Saladi RN, Fox JL (2010) Review: ultraviolet radiation and skin cancer. Int J Dermatol 49(9): 978–86

Diffey BI, Kerwin M, Davis A (1977) The anatomical distribution of sunlight. Br J Dermatol 97(4): 407–10

Elsner P, Holzle E, Diepgen T, et al (2007) Recommendation: daily sun protection in the prevention of chronic UV-induced sun damage — guidelines. J German Soc Dermatol 5(2): 166–73

Farage MA, Miller KW, Elsner P, Maibach H (2008) Intrinsic and extrinsic factors in skin ageing, a review. Int J Cosmet Sci 30: 87–95

Flament f, Bazin R, Laquieze S, Rubert V, Simonpietri E, Piot B (2013) Effect of the sun on visible clinical signs of aging in Caucasian skin. Clin Cosmet Investigational Dermatol 6: 221–32

Helfrich YR, Sachs DL, Voorhees JJ (2008) Overview of skin aging and photoaging. Dermatol Nurs 20(3): 177–83

Kligman AM, Koblenzer C (1997)Demographics and psychological implications for the ageing population. Dermatol Clin 15(4): 549–53

National Cancer Registration and Analysis Service. Non-melanoma skin cancer in England, Scotland, Northern Ireland and Ireland. Available online: www.ncin.org.uk/publications/data_briefings/non_melanoma_skin_

cancer_in_england_scotland_northern_ireland_and_ireland

Primary Care Dermatology Society (2018) PCDS actinic keratosis guideline. Management of actinic keratosis in primary care. Available online: www.guidelines.co.uk/skin-and-wound-care/pcds-actinic-keratosis-guideline/250776.article

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