The Summer Skin Check

Pictorial essay • CLINICAL PRACTICE The summer skin check

Belinda Welsh, MBBS, MMed, FACD, is consultant dermatologist, St Vincent’s Hospital, Melbourne, Skin and Cancer Foundation, Carlton, and is in private practice, Sunbury, Victoria.

BACKGROUND Skin cancer is a major public health problem in Australia and represents a substantial health cost. General practitioners provide the majority of care to patients with skin cancer, so becoming familiar with the clinical features and management of these tumours is important.

OBJECTIVE To provide a pictorial essay on the common types of benign and malignant skin lesions encountered in general of suspicion is necessary in this population in women, the neck, shoulders and outer practice, and briefly describe key clinical • exposure to arsenic is a known risk factor arms are also sites of predilection4 features, differential diagnosis and for the development of basal cell carci- • scars should be checked for evidence of management options. noma (BCC)2 and Bowen disease3 recurrence of previously excised lesions - •a history of change or symptomatology in BCCs may develop within longstanding DISCUSSION any lesion – skin cancers are changing scars and ulcers5,6 Examination for skin cancer should be lesions and the time course for this change • lymph nodes should be assessed for the considered in the general practice setting is generally evident over a period of months. early detection of metastatic disease if for all patients over the age of 40 years, there is a history of melanoma or squa- particularly the elderly. A proper skin check Examination mous cell carcinomas (SCCs). requires a systematic approach and ideally The following factors are important in examination: an entire consultation should be set aside • good lighting, preferably natural light Management for this purpose. However, clinical • magnification – a dermatoscope can be Biopsy of a lesion (punch or shave) is advisable examination conducted for other purposes helpful in diagnosis of both melanocytic when a firm clinical diagnosis cannot be made or provides an opportunity for screening and and nonmelanocytic lesions when the treatment choice may be dictated by early detection of skin cancer. • positioning – patients should be the tumour type or pattern of growth. Multiple 2 undressed to their underwear, so a warm mm punch biopsies may be necessary to define History taking room or blanket for comfort is desirable. poorly demarcated tumours. Tailor each manage- Having the patient lie on the examination ment decision to the particular lesion in the The following points in history taking can help couch can be useful so the soles of the individual patient. In general, simple surgical exci- identify high risk patients: feet are not missed sion with primary closure is the treatment of • blistering sunburns • look closely – gently stretching the skin choice for most skin cancers, although some • occupational and recreational exposure to can often make BCCs more obvious. anatomical areas require particular care (Table 1) solar radiation • palpate – dermatofibromas for example and specialist referral may be desirable for tech- • family or personal history of melanoma or have a characteristic feel on palpation nically difficult excisions. Prevention should be multiple atypical (dysplastic) naevi • concentrate on high risk areas – the emphasised (Table 2) and changes to look for in • family or personal history of non- highest rates for NMSC are found on the suspicious lesions discussed. Follow up is rec- melanoma skin cancer (NMSC) face, especially the nasolabial fold, eyelid ommended for three reasons: detection of •immunosuppression – higher rates and and the nonmucosal skin of the lip fol- further primary tumours, detecting local persis- earlier onset of skin cancer is present in lowed by the ears, nose and cheek. In tence of previously treated tumours, and early transplant patients,1 therefore a high index men, the neck, back and shoulders, and detection of metastatic disease.

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Recurrence after excision is not Table 1. Problem areas uncommon as clinical margins are often requiring care in management underestimated

Face – for cosmetic reasons and the possibility of nerve damage Eyelids – scarring can cause entropion Lips and helix of the ear – because of malignant potential Neck – where the accessory nerve is Figure 2. Seborrhoeic keratosis superficial Fingers – function is a major consideration later thickening to become brownish-black. Lower limb – healing can be very slow The surface is irregular and shows minute pits. Management Figure 4. Porokeratosis Table 2. Recommendations for When flat and pigmented, seborrhoeic ker- prevention of skin cancer atoses may require biopsy to differentiate Porokeratoses them from lentigo maligna melanoma. These can be removed with a number of destructive Clinical features Where possible use clothing as the techniques such as cryotherapy, curettage, primary means of photoprotection – electrosurgery or shave excision. Porokeratoses (Figure 4) are uncommon, dis- preferably closely woven fabrics that aren’t transparent when held up to tinctive, benign lesions due to clones of the light Multiple eruptive seborrhoeic epidermal cells that show varying degrees of Wear hats and sunglasses keratoses are rare but may be a sign of dysplasia. They develop as annular dry internal malignancy (Leser-Trelat sign) plaques surrounded by a raised fine keratotic Seek shade. Avoid the sun in the middle of the day wall. Porokeratoses may be isolated or multiple and most often appear on the limbs. Use sunscreen – broad spectrum SPF15 or greater should be applied to Management all exposed areas of the skin as a last line of defence. Reapply every 2 hours None usually needed. If lesions are hyperkera- Advise against the use of sunbeds, totic or multiple, cryotherapy may be performed. tanning booths and tanning lamps The rare giant forms may be premalignant

Figure 3. Dermatofibroma Dermatofibroma Clinical features Dermatofibroma (Figure 3) are benign tumours of fibroblasts that are firm, solitary Figure 1. Seborrhoeic keratosis dermal nodules usually found on the limbs of Figure 5. Solar keratosis younger people. They have an ‘iceberg’ effect Seborrhoeic keratoses in that they feel larger than they look. The Clinical features overlying epidermis is often lightly pigmented Solar keratoses and dimples when the nodule is squeezed. Seborrhoeic keratoses (Figure 1, 2) are very Management Solar keratoses (Figure 5) are common common benign tumours usually found on the lesions associated with dysplasia, particularly face and trunk. They develop gradually as No treatment is usually necessary, although within basal keratinocytes. They represent a slightly elevated, ovoid yellow-brown, well biopsy may be performed if the diagnosis potential precursor of SCC, although only a defined papules with a greasy appearance, is uncertain. small percentage evolve into invasive SCCs.

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Clinical features to invasive SCC has not been established, Differential diagnosis but appears to be low.7 Solar keratoses are found on the chronically Differential diagnosis • SCC sun exposed sites of the head and neck, • Atypical fibroxanthoma dorsa of the hands, and the forearms, and • Superficial BCC • Merkel cell carcinoma present as erythematous macule with super- • Psoriasis • Amelanotic melanoma. imposed hyperkeratosis. Solar keratoses are • SCC Management options generally multiple and may be confluent. • If pigmented, may mimic superficial Differential diagnosis spreading melanoma. • Partial biopsy will almost always be Management options reported as a well differentiated SCC as Bowen disease, SCC, solar lentigo or lentigo pathology requires the entire architecture maligna if pigmented. • Surgical excision to suggest the possibility of keratoacan- Management options • Cryotherapy thoma. If in doubt, treat as a SCC • Imiquimod • Curettage +/- cryotherapy •No treatment • 5-flurouracil • Shave excision • Cryotherapy • Curettage and diathermy • Surgical excision • 5-flurouracil • Photodynamic therapy • Intralesional methotrexate • Imiquimod • Superficial radiotherapy • Superficial radiotherapy. • Curettage • Laser ablation. • Laser resurfacing. Extra caution is required in Due to extension of keratinocyte atypia, immunosuppressed patients as keratoa- Thickening and tenderness on down hair follicles recurrence after canthomas may progressively grow lateral palpation are indicators of possible treatment with superficial modalities rather than involute10 transformation into invasive SCC (eg. cryotherapy) can occur, particularly on the face

Figure 8. Squamous cell carcinoma

Figure 6. Bowen disease Figure 7. Keratoacanthoma Bowen disease Bowen disease (intraepidermal SCC) (Figure Keratoacanthoma 6) is associated with full thickness epidermal dysplasia with follicular involvement and is Keratoacanthoma (Figure 7) are lesions that classified as an intraepidermal SCC. Despite can be thought of as a well differentiated this, they tend to have a prolonged in-situ forms of SCC characterised by spontaneous Figure 9. Squamous cell carcinoma phase that may last many years. resolution. Clinical features Clinical features Squamous cell carcinoma Longstanding, slowly enlarging lesions that Keratoacanthoma are most common on the are generally asymptomatic with a predilec- chronically exposed sites of the head, neck, Squamous cell carcinomas (Figure 8, 9) are tion for the lower legs (especially in females) hands, and forearms. They rapidly enlarge over characterised by lobular proliferation of ker- but may occur at any site. Lesions are a a period of 4–8 weeks to form a tender, erythe- atinocytes with intradermal invasion and sharply defined, round to oval, erythematous matous nodule with a central keratotic plug. prominent keratin production. The majority of hyperkeratotic plaque. The degree of hyperk- Resolution takes 6–12 weeks, sometimes SCCs are thought to arise from solar keratoses.8 eratosis may vary. The rate of transformation leaving a scar. A minority will persist as SCC.

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Clinical features Superficial multifocal BCC • Amelanotic nodular melanoma. Management options Squamous cell carcinomas are characterised by Clinical features tender erythematous papules or nodules, with a Superficial BCCs generally occur on the trunk • Surgical excision variable amount of hyperkeratosis enlarging and limbs, are bright pink and shiny, and usually • Superficial radiotherapy over a period of months, usually with associ- well defined erythematous macular lesion • Intralesional interferon alfa ated tenderness. Bleeding and ulceration may (Figure 10). Stretching the skin will highlight a • Imiquimod develop and the risk of metastasis increases thread-like pearly rim or islands of pearliness • Photodynamic therapy. with tumour thickness, clinical immunosuppres- throughout the lesion. There is progressive sion and poorly differentiated tumours.9 enlargement over months to years but ulcera- Differential diagnosis tion and bleeding is uncommon. With time, areas of nodular or even sclerosing growth • Hyperkeratotic solar keratosis or Bowen pattern may supervene. Recurrence is common. disease – clinical diagnosis can be difficult Differential diagnosis in the early stages • Nodular basal cell carcinoma • Bowen disease • Amelanotic melanoma • Solar keratosis • Atypical fibroxanthoma – particularly if on • Psoriasis the scalp. • Eczema. Management options Management options

• Surgical excision • Cryotherapy Figure 12. Morphoeic BCC • Superficial radiotherapy. • Imiquimod • 5-flurouracil Beware tumours located on lips, ears or • Photodynamic therapy Morphoeic BCC scalp as they have a higher risk of early • Surgical excision Histology metastasis usually to local lymph nodes9 • Curettage and diathermy • Superficial radiotherapy. Morphoeic lesions have a sclerosing growth pattern with fibrosis surrounding areas of Basal cell carcinomas BCC (Figure 12). Clinical features Basal cell carcinomas (BCCs) are tumours derived from basal keratinocytes. Their onset Morphoeic lesions present mostly on the is insidious. In months or years they extend head and neck and can be clinically difficult to peripherally as well as in depth and are detect. They are often indurated to palpation, capable of destroying cartilage and bone. are frequently asymptomatic and tend to look Metastases rarely develop from BCCs,11 the like a pale scar. Morphoeic lesions are usually main risk being recurrence after incomplete longstanding and tend to be deeply invasive. removal. There are three common growth Differential diagnosis patterns of BCC (superficial multifocal, Figure 11. Nodular BCC nodular and morphoeic) that have a distinc- Major differential diagnosis is a scar and tive clinical presentation. Any of these may Nodular BCC biopsy is necessary to establish the diagnosis. also show ulceration or pigmentation. Clinical features Management options Nodular BCCs (Figure 11) are more often • Consider referral for specialist care found on the head and neck. They are a • Moh’s micrographic surgery shiny, translucent (pearly), telangiectatic • Superficial radiotherapy. papule or nodule. Recurrent ulceration is frequent and pigmentation may suggest Morphoeic lesions need to be treated melanoma. with respect as they can have extensive Differential diagnosis subclinical extension and perineural invasion particularly when located around • Nonpigmented intradermal naevi the eyes, ears and nose. Recurrence is • Neuromas frequent due to incomplete excision Figure 10. Superficial BCC • SCC

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Although often conspicuous, ink spot lentigo are benign lesions Table 3. Margins of re-excision for melanoma after initial excisional biopsy

Tumour thickness Margin of re-excision In situ (level 1) 0.5 cm ≤2.0 mm 1.0 cm >2.0 mm 2.0 cm Figure 13. Solar lentigo Solar lentigo Clinical features

Solar lentigo (Figure 13) represent a macular area of pigmentation appearing after either acute or chronic sun exposure. Histologically there is a linear increase of melanocytes at the dermoepidermal junction without cyto- Figure 15. Atypical naevi logic atypia. Backs of the hands, face and shoulders are common sites. Over time they may evolve into seborrhoeic keratoses. Atypical naevi Figure 16. Lentigo maligna melanoma Management options Clinical features 3 lists recommended excision margins. The • Cryotherapy can lighten solar lentigo, but Atypical (dysplastic) naevi (Figure 15) are four most common subtypes are: care should be taken in olive skinned usually larger than ordinary naevi, predomi- Lentigo maligna melanoma patients as they may hyperpigment nate on the trunk and often showing a • Laser. mixture of tan, dark brown and pink areas. Lentigo maligna melanoma (Figure 16) account The surface texture is often ‘pebbly’ and the for 5–15% of all melanomas and occur mainly Shave biopsy may be necessary to distin- border ‘smudgy’. The term atypical naevus on the exposed skin of the elderly. An irregu- guish solar lentigo from lentigo maligna syndrome refers to the occurrence of multi- larly pigmented and shaped macule (lentigo or superficial spreading melanoma ple (up to 80 or more) dysplastic naevi in an maligna/Hutchinson melanotic freckle) may individual. Melanoma risk is increased in have been enlarging slowly for many years as these patients12 with the risk increased an in-situ melanoma before an invasive nodule further in melanoma prone families with atyp- (lentigo maligna melanoma) appears. 13 ical mole syndrome. Differential diagnosis Management • Solar lentigo Surveillance (baseline photography and • Flat pigmented seborrhoeic keratosis. regular 6–12 month follow up) enables early Management options diagnosis of melanoma. This is much more cost effective in preventing life threatening • Shave biopsy of the lesion’s centre is rec- melanoma than prophylactic excision of atypi- ommended if there is diagnostic cal naevi.14 uncertainty Figure 14. Ink spot lentigo • Surgical excision Ink spot lentigo Due to the increased risk of melanoma • Superficial radiotherapy. in these patients regular follow up is Superficial spreading melanoma Ink spot lentigo (Figure 14) are small (less necessary for life than 5 mm) densely black macules, usually Superficial spreading melanoma account for on sun exposed skin. They can be cause for 50–75% of all melanomas and may develop concern because of their dark colour and Melanoma on any part of the body (Figure 17) at any irregular lateral margin. Melanocyte numbers Patients are often most concerned about pig- age. They have variegated colour and an and melanin production are increased in mented lesions because of the possibility of irregular expanding margin. these lesions but there is no cellular atypia. melanoma and its capacity to be lethal. Table

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Partial biopsy of the suspected melanoma Invest Dermatol 1961;37:317–332. should be avoided as this will interfere 4. Buettner PG, Raasch BA. Incidence rates of skin cancer in Townsville, Australia. Int J Cancer with accurate histological staging 1998;78:587–593. 5. Burns DA, Calnan, CD. Basal cell epithelioma in a chronic leg ulcer. Clin Exp Dermatol 1978;3:443–445. 6. Hendricks WM. Basal cell carcinoma arising in a chicken pox scar. Arch Dermatol 1980; 116:1304–1305. 7. Kao GF. Carcinoma arising in Bowen’s disease. Arch Dermatol 1986;122:1124–1126. Figure 17. Superficial spreading melanoma 8. Mackie R. An illustrated guide to the aetiology, clinical features, pathology and management of Differential diagnosis benign and malignant cutaneous tumours. London: Martin Dunitz Ltd, 1989. 9. Rowe DE, Carroll RJ, Day CLJ. Prognostic • Atypical (dysplastic) naevus factors for local recurrence, metastasis, and sur- • Pigmented BCC Figure 18. Nodular melanoma vival rates in squamous cell carcinoma of the • Pigmented seborrhoeic keratosis skin, ear and lip. Implications for treatment modality selection. J Am Acad Dermatol • Haemangioma. 1992;26:976–990. Management 10. Cohen EB, Komorowski RA, Clowry LJ. Cutaneous complications in renal transplant • Surgical excision. recipients. Am J Clin Pathol 1987;88:32–37. 11. Lo JS, Snow SN, Reizner GT, Mohs FE, Larson Nodular melanoma PO, Hruza GJ. Metastatic basal cell carcinoma: report of 12 cases with a review of the litera- Nodular melanoma represent 15–35% of all ture. J Am Acad Dermatol 1991;24:715–719. melanomas and appear as a pigmented (or 12. Kang S, Barnhill RL, Mihm MC Jr, et al. occasionally flesh coloured) amelanotic Melanoma risk in individuals with clinically nodule with no antecedent in-situ phase atypical naevi. Arch Dermatol 1994;30:999–1001. (Figure 18). It is the most rapidly growing and Figure 19. Acral lentiginous melanoma 13. Carey WP Jr, Thompson CJ, Synnestvedt M, et aggressive type of melanoma. al. Dysplastic naevi as a risk factor for Differential diagnosis melanoma in patients with familial melanoma. Acknowledgment Cancer 1994;74:3118–3125. • Pigmented BCC Thanks to Professor Robin Marks from St Vincent’s 14. Kelly JW, Yeatman JM, Regalia C, Mason G, Henham AP. A high incidence of melanoma • SCC or pyogenic granuloma if amelanotic. Hospital Melbourne and Associate Professor John Kelly, Victorian Melanoma Service, Alfred Hospital, found in patients with multiple dysplastic naevi Management Melbourne, for kindly allowing reproduction of by photographic surveillance. Med J Aust some of the clinical images in this article. 1997;167:191–194. AFP • Surgical excision. Suggested reading Acral lentiginous melanoma National Health and Research Medical Council. Acral lentiginous melanoma represent 5–10% Clinical Practice Guidelines. Nonmelanoma skin cancer: guidelines for treatment and management of all melanomas and occur on the palmar, in Australia. Canberra: Commonwealth of Australia, plantar and subungal skin (Figure 19). Although 2003. Available through Ausinfo Government Info rare in caucasians, they are particularly bookshops Australia wide, phone toll free 132 447 common in both the Chinese and Japanese or at: www.noie.gov.au/projects/egovernment/ population. Better_Information/infoaccessnetwork/index.html Differential diagnosis Conflict of interest: none declared.

•Melanocytic naevus References • Subungal heamatoma 1. Bouwes Bavinck JN, Hardie DR, Green A, et al. • Talon noir – a pigmented petechial area The risk of skin cancer in renal transplant recipients in Queensland, Australia. A follow up on the heel following minor trauma. study. Transplantation 1996;61:715–721. Management 2. Mowad CM, Jaworsky C, Werth VP. Numerous erythematous truncal plaques. Multiple basal • Surgical excision. cell carcinomas associated with arsenic inges- tion. Arch Dermatol 1996;132:1105–1109. 3. Graham HJ, Mazzanti GR, Helwig GB. Chemistry Correspondence of Bowen’s disease: Relationship to arsenic. J Email: [email protected]

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