Symptoms and signs	Diagnostic significance
1. Lump in or on the skin Size, shape and surface features Revealed by inspection—is the lesion smooth-surfaced, irregular, exophytic (i.e. projecting out of the surface)?	Epidermal lesions such as warts usually have a surface abnormality but deeper lesions are usually covered by normal epidermis. A punctum suggests the abnormality arises from an epidermal appendage, e.g. epidermal (sebaceous) cyst
Depth within the skin Superficial and deep attachments Which tissue is the swelling derived from?	Tends to reflect the layer from which lesion is derived and therefore the range of differential diagnosis (i.e. epidermis, dermis, hypodermis or deeper)
Character of the margin Discreteness, tethering to surrounding tissues, three-dimensional shape	A regular shaped, discrete lesion is most likely cystic or encapsulated (e.g. benign tumour). Deep tethering implies origin from deeper structures (e.g. ganglion). Immobility of overlying epidermis suggests a lesion derived from skin appendage (e.g. epidermal cyst)
Consistency Soft, firm, hard, ‘indurated’, rubbery	Soft lesions are usually lipomas or fluid-filled cysts. Most cysts are fluctuant unless filled by semi-solid material (e.g. epidermal cysts), or the cyst is tense (e.g. small ganglion) Malignant lesions tend to be hard and irregular (‘indurated’) with an ill-defined margin due to invasion of surrounding tissue Bony-hard lesions are either mineralised (e.g. gouty tophi) or consist of bone (e.g. exostoses)
Pulsatility	Pulsatility is usually transmitted from an underlying artery which may simply be tortuous or may be abnormal (e.g. aneurysm or arteriovenous fistula)
Emptying and refilling	Vascular lesions (e.g. venous malformations or haemangiomas) empty or blanch on pressure and then refill
Transilluminability	Lesions filled with clear fluid such as cysts ‘light up’ when transilluminated
Temperature	Excessive warmth implies acute inflammation, e.g. pilonidal abscess
2. Pain, tenderness and discomfort	These symptoms often indicate acute inflammation. Pain also develops if a non-inflammatory lesion becomes inflamed or infected (e.g. inflamed epidermal cyst). Malignant lesions are usually painless
3. Ulceration (i.e. loss of epidermal integrity with an inflamed base formed by dermis or deeper tissues)	Malignant lesions and keratoacanthomas tend to ulcerate as a result of central necrosis. Surface breakdown also occurs in arterial or venous insufficiency (e.g. ischaemic leg ulcers), chronic infection (e.g. TB or tropical ulcers) or trauma, particularly in an insensate foot
Character of the ulcer margin	Benign ulcers—the margin is only slightly raised by inflammatory oedema. The base lies below the level of normal skin Malignant ulcers—these begin as a solid mass of proliferating epidermal cells, the centre of which eventually becomes necrotic and breaks down. The margin is typically elevated ‘rolled’ and indurated by tumour growth and invasion
Behaviour of the ulcer	Malignant ulcers expand inexorably (though often slowly), but may go through cycles of breakdown and healing (often with bleeding)
4. Colour and pigmentation Normal colour	If a lesion is covered by normal-coloured skin then the lesion must lie deeply in the skin (e.g. epidermal cyst) or deep to the skin (e.g. ganglion)
Red or purple	Redness implies increased arterial vascularity, which is most common in inflammatory conditions like furuncles. Vascular abnormalities which contain a high proportion of arterial blood such as Campbell de Morgan spots or strawberry naevi are also red, whereas venous disorders such as port-wine stain are darker. Vascular lesions blanch on pressure and must be distinguished from purpura which does not
Deeply pigmented	Benign naevi (moles) and their malignant counterpart, malignant melanomas, are nearly always pigmented. Other lesions such as warts, papillomata or seborrhoeic keratoses may become pigmented secondarily. Hairy pigmented moles are almost never malignant. Rarely, malignant melanomas may be non-pigmented (amelanotic). New darkening of a pigmented lesion should be viewed with suspicion as it may indicate malignant change
5. Rapidly developing lesion	Keratoacanthoma, warts and pyogenic granuloma may all develop rapidly and eventually regress spontaneously. When fully developed, these conditions may be difficult to distinguish from malignancy. Spontaneous regression marks the lesion as benign
6. Multiple, recurrent and spreading lesions	In certain rare syndromes, multiple similar lesions develop over a period. Examples include neurofibromatosis and recurrent lipomata in Dercum’s disease. Prolonged or intense sun exposure predisposes a large area of skin to malignant change. Viral warts may appear in crops. Malignant melanoma may spread diffusely (superficial spreading melanoma) or produce satellite lesions via dermal lymphatics
7. Site of the lesion	Some skin lesions arise much more commonly in certain areas of the body. The reason may be anatomical (e.g. pilonidal sinus, external angular dermoid or multiple pilar cysts of the scalp) or because of exposure to sun (e.g. solar keratoses or basal cell carcinomas of hands and face)
8. Age when lesion noticed	Congenital vascular abnormalities such as strawberry naevus or port-wine stain may be present at birth. Benign pigmented naevi (moles) may be detectable at birth, but only begin to enlarge and darken after the age of 2

History and examination

As the patient describes the problem, the lesion is usually offered for examination which may guide the direction and emphasis of history taking. The patient should be questioned about sun exposure and about other similar lesions or any regional lumps. Detailed inspection and palpation follow, leading to a diagnosis or narrow differential diagnosis.

A general history must be taken to ascertain any relevant systemic symptoms (e.g. weight loss), concurrent disorders (e.g. diabetes predisposes to infection and influences surgical management), a history of previous similar lesions, surgical treatment or trauma to the area. For example, a history of rodent ulcers (basal cell carcinoma) makes this diagnosis more likely next time. Previous surgery or trauma can lead to implantation epidermoids or a chronic inflammatory response to a foreign body.

Family history is valuable in rare genetic disorders such as neurofibromatosis and tuberous sclerosis. Social history should include occupational details. For example, natal cleft pilonidal sinus is more common in truck drivers. Exposure to carcinogens such as lubricating oils persistently spilt on clothing may cause squamous carcinoma. Outdoor workers, especially in the tropics, are predisposed to all skin cancers. Chronic ulcers may be contracted during foreign travel, e.g. tropical ulcers, Madura foot, tuberculous or atypical mycobacterial ulcers. Patients sometimes deliberately injure themselves, producing odd chronic ‘artefactual’ lesions; a psychiatric history is valuable here, though rarely forthcoming.

Drug history is rarely relevant, though agents applied topically, e.g. silver nitrate stick, caustic agents and contact dermatitis to adhesive dressings can distort the clinical picture. Check if the patient is taking warfarin or aspirin since they may increase the risk of perioperative haemorrhage.

The lesion is examined in detail, looking for the points in Table 46.1. General clinical examination searches for other similar lesions, regional lymphadenopathy or a primary malignancy arising elsewhere and metastasising to skin. For example, if inguinal lymph nodes are enlarged, rectal and genital examination should be carried out to exclude concealed carcinoma. The lower limbs, including the soles of the feet, should also be examined for malignant melanoma.

Principles of managing skin lesions

Many skin lesions can be diagnosed from the history and clinical examination, but where there is doubt, biopsy is needed, particularly if there is risk of malignancy. Excision biopsy is treatment if the lesion is small. Incision and excision biopsy techniques are illustrated in Chapter 10, p. 136 and Box 46.1 summarises surgical options for skin conditions.

Box 46.1 Principles of management of ‘surgical’ skin lesions

Simple excision or other physical methods, e.g. electrocautery, laser therapy or cryotherapy—for small, obviously innocent lesions

Excision biopsy—if there is any risk of malignancy or the clinical diagnosis is doubtful (only for small lesions)

Biopsy—for large lesions. Definitive therapy is then planned according to the histology

Wide local excision with or without skin grafting—for malignant melanomas and sometimes for other large malignant lesions

Radiotherapy—an alternative to excision for basal cell carcinoma and primary squamous cell lesions. Also sometimes used if regional lymph nodes are involved in squamous cell carcinoma

Topical chemotherapy—with 5-fluorouracil cream for certain skin malignancies

Photodynamic therapy—for certain skin malignancies. Malignant cells absorb a photosensitising chemical which reacts with light of a particular wavelength to destroy the cells

Surgical lymph node clearance—if nodes are involved by malignant melanoma or squamous carcinoma

For axillary hyperhidrosis, the most effective and least risky option is injections of botulinum toxin into axillary skin. This needs to be repeated at 6–9-monthly intervals. Local excision of axillary sweat glands is another popular surgical option. For palmar hyperhidrosis unresponsive to dermatological management, thoracoscopic destruction of upper thoracic sympathetic nerves is highly effective.

Lesions originating in the epidermis

Benign epidermal lesions

Skin tags (squamous cell papillomas)

Skin tags are small benign polypoid lesions up to 5 mm across consisting of loose connective tissue covered by normal, often pigmented, keratinised epithelium. Common in adults, they may occur anywhere, particularly the trunk, neck, axillae and groins; they may be irritated by clothing and bleed. Lesions are easily removed by cryotherapy (freezing), cautery or excision (under local anaesthesia), or by tying a fine thread around the stalk (also under local anaesthesia) which leads to ischaemic atrophy.

Warts

Warts are small, virus-induced epidermal tumours characterised pathologically by irregular thickening of the epidermis with excessive keratinisation and exaggerated dermal papillae. The morphology depends on the location.

The common wart (verruca vulgaris), a papilliferous lesion up to 1 cm in diameter, is most often found on the fingers and back of the hands. In children, warts are often multiple and can occur on the face. Facial lesions are often less keratotic with a smoother, more dome-like shape. They are often called juvenile or plane warts (verruca plana juvenilis). Lesions on the sole of the foot, plantar warts (verruca plantaris), become very keratotic and flattened by pressure. They may extend deeply into the foot, causing pain. Warts may also occur on the genitalia, perineum and perianal area. These originate with papilloma virus infection and are usually spread by sexual contact. Genital warts sometimes grow to a large size and are then known as condylomata acuminata.

Warts are frequently seen in immune-suppressed patients. They grow and regress spontaneously over several months, but often require treatment to relieve pain, irritation or inconvenience or for aesthetic reasons. Keratolytic applications (salicylic acid or podophyllin resin preparations), cryosurgery (liquid nitrogen application) or topical imiquimod are often the first choice of treatment. If unsuccessful, electrocautery (with or without curettage) and simple excision can be used.

Seborrhoeic keratosis

Seborrhoeic keratoses (seborrhoeic warts) are very common in elderly patients but occasionally appear in younger people (Fig. 46.2). They are most common on the trunk, face, neck and arms, often with many different sized lesions with varying pigmentation. They may be up to several centimetres in diameter. The lesions are slightly raised, sharply demarcated and plaque-like; they look and feel irregular and waxy. Darkly pigmented lesions cannot be distinguished clinically from superficial spreading malignant melanomas.

Fig. 46.2 Seborrhoeic keratoses

Histologically, a seborrhoeic keratosis is a localised proliferation of the epidermal basal layer. There is often hyperkeratosis in surface crypts, resulting in round keratin nests. Seborrhoeic keratoses are sometimes called basal cell papillomas, but are not true neoplasms and are unrelated to basal cell carcinoma.

Treatment is only required for unsightly or easily traumatised lesions. As they are so superficial, they can be ‘scraped off’ with a curette or scalpel under local anaesthesia. Cryotherapy is used but caution is needed in patients with dark skin, since enthusiastic cryotherapy can lead to permanent loss of pigmentation.

Keratoacanthoma

Keratoacanthoma is a nodular, single skin lesion, up to 2 cm across (Fig. 46.3b, c). They have an irregular central crater containing keratotic debris. The histological lesion consists of localised tumour-like epidermal proliferation, with a thick prickle cell layer (acanthosis) and marked keratinisation. Some epithelial cells are large with atypical nuclei; the underlying dermis exhibits chronic inflammatory cell infiltration.