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Solar damage, moles, solar keratoses and skin cancer

Solar damage, moles, solar keratoses and skin cancer

Non-neoplastic solar damage

Sunlight induces changes in the skin, often described as premature ageing, which are well recognised in the Australian community. The changes include wrinkling, thickening or thinning of the skin, hyperpigmentation, hypopigmentation and telangiectasia. These are most marked on the areas that are heavily exposed to sunlight, eg the face, back of the hands, neck and upper trunk. They are induced predominantly by the ultraviolet (UV) component of sunlight. They are non-neoplastic in themselves and do not have a malignant potential.

Prevention of solar damage is the best approach.

           Reduce sunlight exposure by wearing hats and protective clothing.

           Avoid the sun around the middle of the day – at least 60% of ultraviolet B (UVB) radiation occurs between the hours of 10am to 2pm (11am to 3pm summer time).

           Seek shade whilst outdoors.

           Use a broad-spectrum sunscreen with a sun protection factor (SPF) of 15 or more, see Sunscreens.

The treatment depends on the extent of the existing damage. Mild solar elastosis with associated xeroderma (dry skin) can be treated with emollients. For moderate damage, use

tretinoin 0.025 to 0.05% cream or gel OR alpha-hydroxy acid 5% cream.

For severe damage, superficial chemical, surgical or laser skin peels are recommended.

Melanocytic naevi (moles)

Melanocytic naevi are localised collections of naeval melanocytes in the epidermis and dermis. The majority are believed to be induced by exposure to sunlight in people who are predisposed to develop them. The malignant potential of individual lesions is very low and prophylactic excision to prevent malignant transformation is not advised. However, large numbers of naevi, both common acquired naevi and dysplastic naevi, are a risk factor for melanoma. A substantial proportion of melanomas arise de novo in the absence of any clinical or histological evidence of a pre-existing naevus. The vast majority of naevi are banal, common acquired melanocytic naevi. These naevi are even in colour, with a regular shape and border.

Most melanocytic naevi do not require treatment. Destructive therapy of melanocytic naevi without histological assessment is to be condemned. If treatment is required, histological assessment of the whole lesion is essential to confirm that a malignant lesion has not been removed.

Excision is the treatment of choice for a pigmented lesion where there is doubt about malignancy. A 2 to 3mm margin of normal skin around the lesion should be taken in the primary excision. If there is a very large pigmented lesion where excision biopsy could create problems, eg facial lentigo maligna, incisional biopsy is acceptable. This does not affect the prognosis, even when histology may show the lesion to be a melanoma and further excision is required.

There is an increased risk of melanoma, which correlates with the number of melanocytic naevi, particularly more than one hundred naevi. Clinical photographs are useful for monitoring patients with large numbers of naevi. People at high risk of melanoma should be advised of specific changes indicating the risk of malignant change and should be encouraged to examine their skin on a regular basis.

People at very high risk of melanoma (those with all of the following features: multiple dysplastic naevi; a family history of dysplastic naevi; and a history of melanoma in themselves or first-degree relatives) need regular surveillance at intervals determined by the frequency of change on comparison with previous photographs.

Follow up for individuals at very high risk should be at 6- to 12-monthly intervals, depending on the frequency with which their naevi have been changing in comparison with photographs. Any new or changing lesion in a patient should be removed if melanoma cannot be easily excluded.

Melanomas may occur in a familial setting. A number of phenotypes have been identified which correlate with an inherited predisposition to melanoma. The classical, first described phenotype is known as the B-K mole syndrome, dysplastic naevus syndrome or familial moles and melanomas syndrome and is quite rare.

In the initial description of the dysplastic naevus syndrome, the B-K moles were 10mm or more in diameter, irregular in outline, a haphazard mixture of tan, black and pink, flat with a small palpable dermal component and strikingly variable from one mole to the next. When biopsied, these moles showed abnormal histology short of melanoma and when followed up, some of these moles became melanomas.

Since then, the word dysplastic naevus has been applied both to moles that have some of the clinical features of B-K moles and to moles that have some of the histological features of B-K moles, but not infrequently normal looking moles can have dysplastic features histologically, whilst dysplastic looking moles can have normal histology. It is now accepted that the clinical appearance of dysplastic moles is used for the purposes of classifying dysplastic naevi and they are referred to as atypical moles.

Patients with many atypical moles who belong to families where other members have many atypical moles, or where there is a family history of melanoma, are likely to carry a melanoma-susceptibility gene. These patients should be enrolled in a formal surveillance program that includes skin photography and regular skin examination.

While these atypical moles may occasionally transform into melanoma, that risk is very small. Prophylactic excision is not required or recommended and they should be excised for diagnostic purposes only, to exclude melanoma. More importantly these moles are markers of risk for the development of melanoma elsewhere on the skin.

A number of candidate genes have been identified for familial melanoma, with or without the presence of dysplastic naevi. Referral to major melanoma treatment centres for genetic counselling and genetic studies should be considered when a strong family history is present.

The presence of more than five atypical moles on a person without familial melanoma has been shown to be a powerful and independent marker of melanoma susceptibility. These patients should be instructed on regular self-examination of their moles to check for any changes.

These are discussed in more detail in Birthmarks.

Seborrhoeic keratoses

Seborrhoeic keratoses are well-defined, evenly pigmented, warty lesions which occur on the head, neck, trunk and limbs in areas not always heavily exposed to sunlight. They commence around the third decade of life, increasing in frequency with increasing age, and are the most common pigmented lesions in people aged 50 years and over. The cause of these lesions is unknown, but sunlight may play a part in the localisation of some of them. They have no malignant potential.

Flat lesions may be difficult to differentiate from a lentigo maligna, particularly on the face or limbs. On occasion lesions may become inflamed, in which case they enlarge and may be pruritic.

Histology reveals keratinocyte hyperplasia with no cytological or other histological evidence of neoplasia.

Seborrhoeic keratoses are benign. The vast majority require no treatment. Where there is doubt about diagnosis, excision by biopsy is necessary to obtain histology. Treatment of lesions for cosmetic purposes, or when they are becoming irritated with trauma from a comb or clothing, includes cryotherapy (when the diagnosis is certain), curettage, shave excision or excision and suture.

Solar keratoses (sun spots)

Solar keratoses are erythematous scaling lesions seen on areas of maximum sunlight exposure such as the face, dorsum of the hands and forearms and lower legs. They can also occur on the upper back. They vary in size from 2 to 10mm in diameter and are normally asymptomatic. They may sting when picked or when exposed to sunlight. They may be more obvious in summer.

These lesions are keratinocyte dysplasias but their potential for malignant transformation is low. They indicate that the person with them has the right skin type and has had enough sunlight exposure to develop a squamous cell carcinoma (SCC), basal cell carcinoma (BCC) or melanoma somewhere. They may remit spontaneously, particularly in people who are in a position to reduce their exposure to sunlight. A SCC on the back of the hand or a BCC on the face, particularly the upper lip, may resemble a solar keratosis.

All patients with solar keratoses should be thoroughly examined to exclude the possibility of a coexisting invasive skin cancer.

Very early, mild lesions may respond to emollients or

salicylic acid 2 to 5% in either aqueous cream or an ointment base for people with very dry skin.

Photoprotection, including use of sunscreens, will lead to remission of mild lesions.

Larger lesions will respond to cryotherapy, cautery or curettage. Where there is doubt about possible malignancy, biopsy is necessary for histopathological examination. If a lesion recurs following cryotherapy, a biopsy should be considered to exclude invasive skin cancer.

In severe cases, initial therapy is with

topical fluorouracil 5% in a cream base applied twice a day for a maximum of 2 weeks on the face or ceased earlier if inflammation becomes severe.

Occasionally, treatment may be extended to 3 to 4 weeks, depending on the need, the degree of inflammation occurring and the site.

For large areas of skin affected with extensive solar keratoses, chemical, surgical or laser peeling is appropriate. In people with a large number of solar keratoses who are at high risk of developing SCC (eg immunosuppressed transplant patients), acitretin [Note] may be of value. A dermatologist is required for the latter two approaches.

Basal cell carcinoma

Basal cell carcinomas are slowly growing invasive epithelial tumours arising from the basal layer of the epidermis. They are the most common skin cancer, with 50% occurring on the head and neck, 30% on the upper trunk and the remainder on the limbs. They have a number of appearances, including a flesh-coloured papule, a rodent ulcer, an erythematous scaling plaque on the trunk and an infiltrating scar-like plaque (morphoeic BCC). Occasionally a BCC may be pigmented, resembling a melanoma. They rarely, if ever, metastasise but can cause extensive local destruction if left untreated. As these tumours are generally slow growing, there is no major urgency required in arranging therapy for BCCs. The following therapies have been used.

Surgical excision has the highest cure rate (95% to 98%) and is the treatment of choice in most situations. Where surgery is not appropriate, eg in the case of multiple lesions, in elderly patients or in people who refuse surgery, other options may be considered. It is used for lesions ranging in size from small to very large. The margin of excision is normally 2 to 3mm, or wider for a morphoeic BCC or large lesions.

Curettage and cauteryis a highly specialised and skilled technique, which is appropriate for relatively small, well-demarcated and relatively superficial tumours. Skill is required, not only in undertaking the technique, but also in selecting the patient and the tumour appropriate for it.

Cryosurgery is a skilled and specialised technique. Used mainly for well-defined superficial spreading BCCs on the trunk. Histological confirmation is required before using this treatment.

Radiotherapy(although rarely used)has a role in treatment of BCCs where surgery is likely to be very destructive, eg around the eyelid, or when the patient is too infirm for surgery. Multiple fractionated doses are required.

Intralesional interferon has been used with success in up to 80% of carefully selected BCCs where surgery or other forms of treatment may cause scarring or sites of poor healing. Examples include a BCC on the chest or leg where a histological diagnosis has been obtained.

Mohs’ microscopically controlled surgery is used for recurrent BCC, or where there is histological evidence of inadequate excision of a tumour with aggressive histological characteristics, particularly around the head and neck, where histological confirmation of clearance of tumour is required before closure of the wound. It provides a high cure rate while preserving normal tissue.

Squamous cell carcinoma

These more rapidly growing keratinocyte tumours are the second most common skin cancers in Australia. They manifest as erythematous scaling proliferative lesions that may grow over months. They may bleed easily and may be tender on palpation. SCCs occur predominantly in areas of the head and neck, limbs and upper trunk heavily exposed to sunlight. Up to 1% may metastasise, with a greater risk of secondary spread occurring in lesions on the ear, lower lip and scalp. A keratoacanthoma is probably a low-risk variant of SCC. Patients with long-term immunosuppression are at increased risk of developing both primary SCCs and metastases.

SCC is a more rapidly growing tumour than BCC and should be treated as soon as is reasonable after the diagnosis is made or suspected. Treatment modalities include surgical excision and radiotherapy.

Surgical excision is the treatment of choice. The margin of excision should be 3 to 5mm around the clinical signs of the tumour.

Radiotherapy may be used for a primary tumour when surgery is likely to be severely scarring or is unsuitable for an elderly or infirm patient. Adjuvant radiotherapy may be used following excision of a high-risk primary tumour, eg a tumour with perineural spread on histopathology.

Metastatic SCC from a primary cutaneous tumour is treated initially with surgical excision, with or without radiotherapy. Cytotoxic chemotherapy may have a limited role in disseminated disease.

For keratoacanthoma, surgical excision is the treatment of choice. Curettage and diathermy may be used if the diagnosis of keratoacanthoma has been histologically confirmed.

Follow up of a patient with primary SCC should occur for at least 2 years after removal of a primary tumour. Clinical examination for signs of possible secondary tumour, eg in the regional lymph nodes, should be undertaken at each follow up visit. Radiological, biochemical and haematological screening are not routine and are indicated only when there is evidence of metastatic disease found on clinical examination.

Melanoma

Melanomas are malignant tumours of melanocytes, which reside in the basal layer of the epidermis. They are initially confined to the epidermis but progress to invade deeper layers, with increasing potential for metastasis as depth of invasion increases. Around 10% of primary cutaneous melanomas will have metastasised by the time the patient presents for treatment. Melanoma is characterised by the clinical description:

Asymmetry. If the lesion is folded in half, the two halves do not fit.

Border irregularity.

Colour variation. Colours include brown, blue, black, red and white.

Diameter enlarging. Change in size of a lesion is a major risk sign.

These signs apply particularly to superficial spreading melanoma, which is the most common type of melanoma. In general it looks like an unusual freckle or mole, different to surrounding lesions and spreading out irregularly in the skin. A nodule may develop in a superficial spreading melanoma or there may be a nodular melanoma arising spontaneously in the absence of a superficial spreading component. Nodular change is associated with increased risk of metastasis.

Superficial spreading and nodular melanomas occur predominantly on the trunk and limbs, not necessarily in sites heavily exposed to sunlight. Lentigo maligna (Hutchinson’s melanotic freckle) is a slowly enlarging pre-invasive melanoma that has all the ABCD characteristics, but occurs on very heavily light-exposed areas in older people. It has the potential to progress to an invasive melanoma and metastasise.

Most melanomas are associated with a history of previous intermittent exposure to sunlight, especially in childhood, sufficient to induce sunburn that is remembered many years later. People with a lentigo maligna (Hutchinson’s melanotic freckle) may give the same history, but they also have a history of very heavy sunlight exposure over many years.

Surgical excision is the treatment of choice for melanoma of all types. Primary excision should include a margin of approximately 3mm of normal skin around a suspicious pigmented lesion.

Views about the margin of normal skin which should be removed following histological confirmation of malignancy are evolving. Current guidelines in Australia are:

           for a melanoma in situ, a margin of 5mm

           for an invasive melanoma up to 1.5mm thick, a margin of 1cm

           for melanoma 1.5 to 4mm thick, a minimum margin of 1cm and a maximum margin of 2cm

           for a melanoma greater than 4mm in thickness, a minimum margin of 2cm.

Lymphatic mapping and selective sentinel node biopsy is a recent surgical technique that may be used in the management of melanomas greater than 1mm thick, since these have an increased risk of regional lymph node metastases. This technique is still under investigation to define its role. Ideally, patients should be treated in carefully controlled trials so that its true value can be determined.

Surgery remains the treatment of choice for metastatic melanoma. Other modalities of therapy, including cytotoxic chemotherapy, immunologically based biological response modifying therapy and radiotherapy, do not offer a great deal of hope in eradication of the disease at the present time but may do so in the future.

Current recommendations for follow up suggest a frequency of review according to the thickness of the primary cutaneous melanoma.

For a tumour less than 1mm thick, 2 years of follow up at 3- to 6-monthly intervals. After that, yearly follow up may be necessary, not only to detect any evidence of metastatic disease, but also because these patients are at higher risk of another primary cutaneous melanoma.

For tumours greater than 1mm thick, follow up is 3- to 4-monthly for the first 2 years, a 6-monthly review until 5 years and then yearly review thereafter. Patients with tumours greater than 4mm thick may require more frequent follow up because of the higher risk of metastatic disease being present.

Clinical examination for signs of secondary disease is all that is required in the vast majority of patients at each follow-up visit. Imaging, biochemical and haematological investigations are not recommended for patients with a primary melanoma of less than 1mm thickness.

In patients with very thick melanomas (>4mm) or with nodal involvement, baseline investigations including imaging, biochemical tests and haematological tests may be of some value for comparison over time.

Prevention of sun-related tumours

Primary prevention is an important part of the public approach to management of SCC, BCC, melanoma, keratoacanthoma, solar keratoses and melanocytic naevi. Reduction of sunlight exposure in childhood is critical, but protection during adulthood is also important.

It has been suggested that the entire spectrum of ultraviolet radiation (UVR), ie 290 to 400nm, contributes to risk of skin cancer, so protection should be broad-spectrum in the UVR range. The primary approach is natural protection, involving the use of good quality clothing and hats whilst outdoors, seeking shade where possible and avoiding the sun around the middle of the day. Reflected radiation may result in people receiving a high dose of UVR even when they are in the shade, and this needs to be accounted for when a canopy is being designed to reduce UVR exposure.

Sunscreens are an adjunct to natural protection, not a substitute for it. The active ingredients in sunscreens work either by absorbing or reflecting UVRTable 1. Absorbent sunscreen chemicals act mainly in the UV range, whereas reflectants provide a barrier across the whole of the terrestrial solar spectrum, including visible light and infra-red radiation. The degree to which they do this is determined by the particular sunscreen active agent and the concentration in the sunscreen product.

Sun protection factor (SPF) is a laboratory-derived figure classifying the relative potency of the different products. Because of the many variables determining the actual dose of UVR received, eg time of day, time of year, cloud cover, reflection, adequacy of application, it is not a figure which can be translated easily into the degree of protection afforded when used under normal conditions outdoors. In other words, SPF numbers should not be translated into burn times for individuals.

The SPF number applies to the ability of a sunscreen product to reduce predominantly the UVB range of the solar spectrum. There is relatively little increase in protection for large increases in SPF number after SPF15, see Table 2, below. Hence, the current public health recommendation is for use of a sunscreen with a SPF of at least 15. Some people with very sun-sensitive skin may feel the need to select a product of SPF30+, the maximum grading currently permissible in Australia.

The current rating of sunscreens includes water resistance and broad-spectrum capacity. A broad-spectrum product under test conditions absorbs at least 90% of ultraviolet A (UVA) radiation in the spectrum of 320 to 360nm. A product rated as water-resistant will state the time for which it is water-resistant and the SPF of the product at the end of the water resistance test period. Current recommendations are that people, particularly those who are swimming or are likely to wash off the product during its use, should choose a product that has both broad-spectrum and water-resistant capacity.

The major contributing factor to the lack of effect of sunscreens is inadequate application, or its removal by touching and wiping after the product has been applied. Therefore the adequacy of initial application of sunscreen and of repeated application during the time outdoors is a very important determinant of effect of the product.

Sunscreens should be applied 15 to 30 minutes before entering the sun and reapplied regularly at 1- to 2-hourly intervals whilst outdoors. An adequate amount of product should be applied to the skin to allow it to be easily spread over the surface of the skin. Around 20g of product would be required for one application to the major exposed parts of the body.

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