Epidermis

The epidermis is comprised of four layers of keratin-producing cells (keratinocytes). It also contains melanocytes, Langerhans cells and Merkel cells. The layers of the epidermis around the eye are described below; cells migrate superficially, undergoing maturation and differentiation through successive layers.

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  Keratin layer (stratum corneum or horny layer) consists of flat cells devoid of nuclei.

  
  
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  Granular cell layer (stratum granulosum) typically consists of one or two layers of flattened cells containing keratohyaline granules.

  
  
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  Prickle cell layer (stratum spinosum) is approximately five cells deep. The cells are polygonal in cross-section and have abundant eosinophilic cytoplasm. Their free borders are united by spiny-appearing desmosomes (cellular junctions).

  
  
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  Basal cell layer (stratum basale) comprises a single row of columnar-shaped proliferating cells containing melanin derived from adjacent melanocytes.

Dermis

The dermis is much thicker than the epidermis. It is composed of connective tissue and contains blood vessels, lymphatics and nerve fibres in addition to fibroblasts, macrophages and mast cells; upward dermal extensions (papillae) interdigitate with downward epidermal projections (rete ridges). In the eyelid the dermis lies on the orbicularis muscle. Adnexa lie deep in the dermis or within the tarsal plates.

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  Sebaceous glands are located in the caruncle and within eyebrow hairs. Tiny sebaceous glands are associated with the thin (vellus) hairs covering periocular skin.

  
  
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  Meibomian glands are modified sebaceous glands found in the tarsal plates. They empty through a single row of 20–30 orifices on each lid. A gland consists of a central duct with multiple acini, the cells of which synthesize lipids (meibum) that form the outer layer of the tear film.

  
  
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  Glands of Zeis are modified sebaceous glands associated with lash follicles.

  
  
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  Glands of Moll are modified apocrine sweat glands opening either into a lash follicle or directly onto the anterior lid margin between lashes; they are more numerous in the lower lid.

  
  
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  Eccrine sweat glands are distributed throughout eyelid skin and are not confined to the lid margin, in contrast to glands of Moll.

  
  
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  Pilosebaceous units comprise hair follicles and their sebaceous glands (see Fig. 1.1A ).

Clinical

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  Macule. Localized area of colour change without infiltration, depression or elevation, less than 1 cm in diameter.

  
  
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  Papule. A solid elevation less than 1 cm in diameter.

  
  
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  Vesicle. Circumscribed lesion containing serous fluid; less than 0.5 cm across.

  
  
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  Bulla. A large (more than 0.5 cm) serous fluid-filled lesion; plural – bullae.

  
  
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  Pustule. A pus-filled elevation less than 1 cm in diameter.

  
  
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  Crust. Solidified serous or purulent exudate.

  
  
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  Nodule. A palpable solid area measuring more than 1 cm.

  
  
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  Cyst. A nodule consisting of an epithelial-lined cavity filled with fluid or semi-solid material.

  
  
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  Plaque. A solid elevation of the skin, greater than 1 cm in diameter.

  
  
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  Scale. Readily detached fragments of shed keratin layer.

  
  
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  Papilloma. A benign neoplastic warty or tag-like projection of the skin or mucous membrane.

  
  
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  Ulcer. A circumscribed area of epithelial loss; in skin an ulcer extends through the epidermis into the dermis.

Histological

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  Tumour strictly refers only to a swelling, though is commonly used to denote a neoplasm.

  
  
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  Neoplasia. Abnormal tissue growth, either benign (localized, non-invasive and non-spreading) or malignant (progressive growth with the potential for distant spread).

  
  
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  Atypia refers to an abnormal appearance of individual cells, e.g. abnormal mitotic figures.

  
  
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  Dysplasia is an alteration of the size, morphology and organization of cellular components of a tissue. There is disturbance of normally structured and recognized layers of tissue (e.g. loss of cell polarity – Fig. 1.1B ).

  
  
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  Carcinoma in situ (intraepidermal carcinoma, Bowen disease) exhibits dysplastic changes throughout the thickness of the epidermis.

  
  
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  Hyperkeratosis. An increase in thickness of the keratin layer that appears clinically as scaling. Hyperkeratosis can be a feature of benign or malignant epithelial tumours.

  
  
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  Acanthosis. Thickening of the prickle cell layer.

  
  
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  Dyskeratosis is keratinization other than on the epithelial surface ( Fig. 1.1C ).

  
  
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  Parakeratosis is the retention of nuclei into the keratin layer ( Fig. 1.1D ).

Pathogenesis

A chalazion (meibomian cyst) is a sterile chronic granulomatous inflammatory lesion (lipogranuloma) of the meibomian, or sometimes Zeis, glands caused by retained sebaceous secretions. Histopathology shows a lipogranulomatous chronic inflammatory picture with extracellular fat deposits surrounded by lipid-laden epithelioid cells, multinucleated giant cells and lymphocytes ( Fig. 1.2A ). Blepharitis is commonly present; rosacea can be associated with multiple and recurrent chalazia. A recurrent chalazion should be biopsied to exclude malignancy.

Chalazion. (A) Histopathology shows a lipogranuloma; the large pale cells are epithelioid cells and the well-demarcated empty space contained fat dissolved out during processing; (B) uninflamed chalazion; (C) acutely inflamed lesion; (D) conjunctival granuloma; (E) marginal chalazion; (F) conjunctival view of chalazion clamp in place prior to incision and curettage

(Courtesy of J Harry and G Misson, from Clinical Ophthalmic Pathology , Butterworth-Heinemann 2001 – fig. A; J Nerad, K Carter and M Alford, from ‘Oculoplastic and Reconstructive Surgery’, in Rapid Diagnosis in Ophthalmology , Mosby 2008 – fig. F)

Diagnosis

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  Symptoms

  
  
  
  
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    Subacute/chronic: gradually enlarging painless rounded nodule ( Fig. 1.2B ).

    
    
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    Acute: sterile inflammation or bacterial infection with localized cellulitis ( Fig. 1.2C ); differentiation may be difficult. A secondarily infected meibomian gland is referred to as an internal hordeolum.

  
  
  
  
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  Signs

  
  
  
  
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    A nodule within the tarsal plate, sometimes with associated inflammation.

    
    
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    Bulging inspissated secretions may be visible at the orifice of the involved gland.

    
    
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    There may be an associated conjunctival granuloma ( Fig. 1.2D ).

    
    
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    A lesion at the anterior lid margin – a marginal chalazion ( Fig. 1.2E ) – may be connected to a typical chalazion deeper in the lid or be due to isolated involvement of a gland of Zeis.

  
  

Treatment

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  Oral antibiotics are required for significant bacterial infection, but not for sterile inflammation.

  
  
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  Conservative. At least a third of chalazia resolve spontaneously so observation may be appropriate, especially if the lesion is showing signs of improvement, though early definitive treatment has been reported to lead to higher patient satisfaction.

  
  
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  Hot compress application several times daily may aid resolution, particularly in early lesions.

  
  
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  Expression. Compression between two cotton-tipped applicators is sometimes effective in expressing the contents of a fresh lesion near the lid margin.

  
  
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  Steroid injection into or around the lesion has been reported to give similar resolution rates to incision and curettage (see below). It may be preferred for marginal lesions or lesions close to structures such as the lacrimal punctum because of the risk of surgical damage.

  
  
  
  
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    Reported regimens include 0.2–2 ml of triamcinolone acetonide aqueous suspension diluted with lidocaine to a concentration of 5 mg/ml, and 0.1–0.2 ml of 40 mg/ml, injected with a 27- or 30-gauge needle.

    
    
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    The success rate following one injection is about 80%; a second can be given 1–2 weeks later.

    
    
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    Local skin depigmentation and fat atrophy are potential but uncommon complications, the risk of which may be reduced by avoidance of infiltration immediately subcutaneously or by utilizing a conjunctival approach.

    
    
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    Retinal vascular occlusion has been described as a complication, probably due to intravascular injection with subsequent embolization.

  
  
  
  
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  Surgery

  
  
  
  
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    Following local anaesthesia infiltration, the eyelid is everted with a specialized clamp ( Fig. 1.2F ), the cyst is incised vertically through the tarsal plate and its contents curetted.

    
    
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    Limited excision of solid inflammatory material (sent for histopathology) with fine scissors may be helpful in some cases, especially if there is no focus of secretions.

    
    
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    A suture should not be used.

    
    
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    Topical antibiotic ointment is used three times daily for 5–7 days following curettage.

  
  
  
  
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  Marginal lesions can be managed by steroid injection, by curettage of an associated deeper chalazion, by shave curettage or by incision and curettage via a horizontal incision on the conjunctival surface or vertically through the grey line.

  
  
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  Prophylaxis

  
  
  
  
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    Treatment of blepharitis, e.g. daily lid hygiene regimen.

    
    
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    Systemic tetracycline may be required as prophylaxis in patients with recurrent chalazia, particularly if associated with acne rosacea.

  
  

Introduction

Xanthelasma (plural – xanthelasmata) is a common, frequently bilateral condition typically affecting middle-aged and elderly individuals. It is a subtype of xanthoma. Hyperlipidaemia is found in about one-third of patients, in whom corneal arcus may also be present. In contrast to chalazion, fat in xanthelasmata is mainly intracellular, with lipid-laden histiocytes (foam cells) in the dermis ( Fig. 1.4A ).

Xanthelasma. (A) Histopathology showing foamy histiocytes within the dermis; (B) large isolated lesion; (C) multiple bilateral smaller lesions

(Courtesy of J Harry – fig. A; S Chen – fig. C)

Diagnosis

Xanthelasmata are yellowish subcutaneous plaques, usually in the medial aspects of the eyelids ( Fig. 1.4B ), commonly bilateral and are multiple ( Fig. 1.4C ).

Treatment

This is principally for cosmesis. Recurrence occurs in up to 50%, and is most common in patients with hypercholesterolaemia.

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  Simple excision is commonly performed where adequate excess skin is present.

  
  
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  Microdissection. Larger lesions can be raised in a flap, the fatty deposits dissected from overlying skin under a surgical microscope using microscissors, and the skin replaced.

  
  
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  Other methods. Good results can be obtained using chemical peeling with bi- or trichloroacetic acid. Laser ablation and cryotherapy have advantages but may be more prone to scarring, including pigmentary changes.

Diagnosis

The clinical appearance and potential for malignant transformation of naevi are determined by their histological location within the skin.

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  Junctional naevus occurs in young individuals as a uniformly brown macule or plaque ( Fig. 1.10A ). The naevus cells are located at the junction of the epidermis and dermis and have a low potential for malignant transformation ( Fig. 1.10B ).

  
  

  
  

  
  

  

  
  

  
  

  Acquired melanocytic naevus. (A) Junctional naevus; (B) histopathology shows heavily pigmented naevus cells at the epidermal/dermal junction; (C) compound naevus; (D) histopathology shows naevus cells both at the epidermal/dermal junction and within the dermis; (E) intradermal naevus; (F) histopathology shows naevus cells within the dermis separated from the epidermis by a clear zone

  
  

  (Courtesy of J Harry – figs B, D and F)

  
  

  
  

  

  
  

  
  

  

  
  

  
  

  

  
  

  
  

  

  
  

  
  

  

  
  
  
  
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  Compound naevus occurs in middle age as a raised papular lesion. The shade of pigment varies from light tan to dark brown but tends to be relatively uniform throughout ( Fig. 1.10C ). The naevus cells extend from the epidermis into the dermis ( Fig. 1.10D ). It has a low malignant potential related to the junctional component.

  
  
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  Intradermal naevus, the most common, typically occurs in older patients. It is a papillomatous lesion, with little or no pigmentation ( Fig. 1.10E ). Histologically, naevus cells are confined to the dermis and have essentially no malignant potential ( Fig. 1.10F ).

  
  
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  Variants of naevi include balloon cell naevi, halo naevi, Spitz naevi (juvenile melanomas) and dysplastic naevi (atypical moles). Multiple dysplastic naevi constitute the dysplastic naevus syndrome (atypical mole syndrome – AMS). Individuals with AMS are at increased risk of developing conjunctival and uveal naevi and cutaneous, conjunctival and uveal melanomas.

Treatment

Treatment is indicated for cosmesis or for concern about malignancy. Excision should be complete in most cases, with at least a 3 mm margin if melanoma is strongly suspected.

Introduction

Port-wine stain (naevus flammeus) is a congenital malformation of vessels within the superficial dermis, consisting histopathologically of vascular spaces of varying calibre separated by thin fibrous septa ( Fig. 1.14A ). About 10% have associated ocular or CNS involvement, including Sturge–Weber (see below) and other defined syndromes.

Port-wine stain. (A) Histopathology shows widely dilated blood-filled spaces separated by fibrous septa; (B) and (C) clinical appearance; ( D–F ) progression of port-wine stain over time, with associated underlying soft tissue hypertrophy

(Courtesy of L Horton – fig. A)

Diagnosis

Port-wine stain manifests clinically as a sharply demarcated soft pink patch that does not blanch with pressure, most frequently located on the face. It is usually unilateral and tends to be aligned with the skin area supplied by one or more divisions of the trigeminal nerve ( Figs 1.14B and C ). Darkening to red or purple takes place with age, and there is commonly associated soft tissue hypertrophy ( Figs 1.14D–F ). Bleeding may occur from focal overlying lobulations (pyogenic granulomas – see below).

Treatment

Treatment with laser (e.g. pulsed-dye) is effective in decreasing skin discoloration; cosmetically superior results are usually achieved by early treatment. Topical preparations such as imiquimod and rapamycin, alone or with adjuvant laser, show promise. Soft tissue debulking is used in a small number of cases. Screening for glaucoma should begin in infancy. Systemic investigation is considered in some patients, particularly those with a lesion of the lumbar area.

Sturge–Weber syndrome

Sturge–Weber syndrome (encephalotrigeminal angiomatosis) is a congenital, sporadic phacomatosis.

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  Port-wine stain , extending over the area corresponding to the distribution of one or more branches of the trigeminal nerve.

  
  
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  Leptomeningeal haemangioma involving the ipsilateral parietal or occipital region may cause contralateral focal or generalized seizures, hemiparesis or hemianopia.

  
  
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  Ocular features may include ipsilateral glaucoma, episcleral haemangioma, iris heterochromia and diffuse choroidal haemangioma (see Ch. 12 ).

Introduction

BCC is the most common human malignancy and typically affects older age groups. The most important risk factors are fair skin, inability to tan and chronic exposure to sunlight. Ninety per cent of cases occur in the head and neck and about 10% of these involve the eyelid. BCC is by far the most common malignant eyelid tumour, accounting for 90% of all cases. It most frequently arises from the lower eyelid, followed in relative frequency by the medial canthus, upper eyelid and lateral canthus. The tumour is slowly growing and locally invasive but non-metastasizing. Tumours located near the medial canthus are more prone to invade the orbit and sinuses, are more difficult to manage than those arising elsewhere and carry the greatest risk of recurrence. Tumours that recur following incomplete treatment tend to be more aggressive.

Histopathology

The tumour arises from the cells that form the basal layer of the epidermis. The cells proliferate downwards ( Fig. 1.18A ) and characteristically exhibit palisading at the periphery of a tumour lobule of cells ( Fig. 1.18B ). Squamous differentiation with the production of keratin results in a hyperkeratotic type of BCC. There can also be sebaceous and adenoid differentiation while the growth of elongated strands and islands of cells embedded in a dense fibrous stroma results in a sclerosing (morphoeic) type of tumour.

Histopathology of basal cell carcinoma. (A) Histopathology shows downward proliferation of lobules of basophilic (purple) cells; (B) palisading of cells at the periphery of a tumour lobule

(Courtesy of J Harry)

Clinical features

Eyelid BCC generally conforms to one of the morphological patterns below.

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  Nodular BCC is a shiny, firm, pearly nodule with small overlying dilated blood vessels. Initially, growth is slow and it may take the tumour 1–2 years to reach a diameter of 0.5 cm ( Figs 1.19A and B ).

  
  

  
  

  
  

  

  
  

  
  

  Clinical appearance of basal cell carcinoma. (A) Early nodular lesion; (B) larger nodular tumour; (C) rodent ulcer; (D) large rodent ulcer; (E) sclerosing tumour; (F) extensive sclerosing tumour

  
  

  
  

  

  
  

  
  

  

  
  

  
  

  

  
  

  
  

  

  
  

  
  

  

  
  
  
  
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  Noduloulcerative BCC (rodent ulcer) is centrally ulcerated with pearly raised rolled edges and dilated and irregular blood vessels (telangiectasis) over its lateral margins ( Fig. 1.19C ); with time it may erode a large portion of the eyelid ( Fig. 1.19D ).

  
  
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  Sclerosing (morphoeic) BCC is less common and may be difficult to diagnose because it infiltrates laterally beneath the epidermis as an indurated plaque ( Figs 1.19E and F ). The margins of the tumour may be impossible to delineate clinically and the lesion tends to be much more extensive on palpation than inspection. On cursory examination a sclerosing BCC may simulate a localized area of chronic blepharitis.

  
  
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  Other types not usually found on the lid are cystic, adenoid, pigmented and multiple superficial.

Introduction

SCC is a much less common, but typically more aggressive tumour than BCC with metastasis to regional lymph nodes in about 20% of cases. Careful surveillance of regional lymph nodes is therefore an important aspect of initial management. The tumour may also exhibit perineural spread to the intracranial cavity via the orbit. SCC accounts for 5–10% of eyelid malignancies and may arise de novo or from pre-existing actinic keratosis or carcinoma in situ (Bowen disease, intraepidermal carcinoma – Fig. 1.20 ). Immunocompromised patients, such as those with acquired immunodeficiency syndrome (AIDS) or following renal transplantation are at increased risk, as are those with a predisposing syndrome such as xeroderma pigmentosum. The tumour has a predilection for the lower eyelid and the lid margin. It occurs most commonly in older individuals with a fair complexion and a history of chronic sun exposure. The diagnosis of SCC may be difficult because certain ostensibly benign lesions such as keratoacanthoma and cutaneous horn may reveal histological evidence of invasive SCC at deeper levels of sectioning.

Carcinoma in situ

(Courtesy of H Frank)

Histopathology

The tumour arises from the squamous cell layer of the epidermis. It is composed of variably sized groups of atypical epithelial cells with prominent nuclei and abundant eosinophilic cytoplasm within the dermis ( Fig. 1.21A ). Well-differentiated tumours may show characteristic keratin ‘pearls’ and intercellular bridges (desmosomes).

Squamous cell carcinoma. (A) Histopathology shows acanthotic squamous epithelium and eosinophilic (pink) islands of dysplastic squamous epithelium within the dermis; (B) nodular tumour with surface keratosis; (C) ulcerating tumour; (D) cutaneous horn

(Courtesy of L Horton – fig. A; A Singh, from Clinical Ophthalmic Oncology , Saunders 2007 – fig. B; H Frank – fig. C; S Farley, T Cole and L Rimmer – fig. D)

Clinical features

The clinical types are variable and there are no pathognomonic characteristics. The tumour may be indistinguishable clinically from a BCC but surface vascularization is usually absent, growth is more rapid and hyperkeratosis is more common.

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  Nodular SCC is characterized by a hyperkeratotic nodule that may develop crusting, erosions and fissures ( Fig. 1.21B ).

  
  
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  Ulcerating SCC has a red base and sharply defined, indurated and everted borders, but pearly margins and telangiectasia are not usually present ( Fig. 1.21C ).

  
  
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  Cutaneous horn with underlying invasive SCC ( Fig. 1.21D ).

Introduction

Keratoacanthoma is a rare, rapidly growing but subsequently regressing tumour that usually occurs in fair-skinned individuals with a history of chronic sun exposure. Immunosuppressive therapy is also a predisposing factor. It is regarded as falling within the spectrum of SCC, and although invasion and metastasis are rare, definitive treatment is usually indicated. Histopathologically, irregular thickened epidermis is surrounded by acanthotic squamous epithelium; a sharp transition from the thickened involved area to normal adjacent epidermis is referred to as shoulder formation ( Fig. 1.22A ); a keratin-filled crater may be seen.

Keratoacanthoma. (A) Histopathology shows irregularly thickened eosinophilic epidermis with a keratin-containing cup and well-marked shoulder formation; (B) hyperkeratotic nodule; (C) large tumour; (D) keratin-filled crater during involution

Diagnosis

A pink dome-shaped hyperkeratotic lesion develops, often on the lower lid ( Fig. 1.22B ), and may double or treble in size within weeks ( Fig. 1.22C ). Growth then ceases for 2–3 months, after which spontaneous involution occurs, when a keratin-filled crater may develop ( Fig. 1.22D ). Complete involution may take up to a year and usually leaves an unsightly scar.

Treatment

Treatment generally involves complete surgical excision with a margin of at least 3 mm, or utilizing Mohs surgery; radiotherapy, cryotherapy or local chemotherapy are sometimes used. Observation is now regarded as inappropriate.

Introduction

Sebaceous gland carcinoma (SGC) is a very rare, slowly growing tumour that most frequently affects the elderly, with a predisposition for females. It usually arises from the meibomian glands, although on occasion it may arise from the glands of Zeis or elsewhere. The tumour consists histopathologically of lobules of cells with pale foamy vacuolated lipid-containing cytoplasm and large hyperchromatic nuclei ( Fig. 1.23A ). Pagetoid spread refers to extension of a tumour within the epithelium, and is not uncommon. Overall mortality is 5–10%; adverse prognostic features include upper lid involvement, tumour size of 10 mm or more and duration of symptoms of more than 6 months.

Sebaceous gland carcinoma. (A) Histopathology shows cells with large hyperchromatic nuclei and vacuolated cytoplasm; (B) nodular tumour; (C) spreading tumour

(Courtesy of A Garner – fig. A; A Singh, from Clinical Ophthalmic Oncology , Saunders 2007 – fig. B; S Tuft – fig. C)

Clinical features

In contrast to BCC and SCC, SGC occurs more commonly on the upper eyelid where meibomian glands are more numerous; there may be simultaneous involvement of both lids on one side (5%).

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  Yellowish material within the tumour is highly suggestive of SGC.

  
  
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  Nodular SGC presents as a discrete, hard nodule, most commonly within the upper tarsal plate ( Fig. 1.23B ), and may exhibit yellow discoloration due to the presence of lipid; it can be mistaken for a chalazion.

  
  
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  Spreading SGC infiltrates into the dermis and causes a diffuse thickening of the lid margin ( Fig. 1.23C ) often with eyelash distortion and loss, and can be mistaken for blepharitis.

Introduction

Melanoma rarely develops on the eyelids but is potentially lethal. Although pigmentation is a hallmark of skin melanomas, half of lid melanomas are non-pigmented and this may give rise to diagnostic difficulty. Features suggestive of melanoma include recent onset of a pigmented lesion, change in an existing pigmented lesion, irregular margins, asymmetrical shape, colour change or presence of multiple colours, and diameter greater than 6 mm.

Lentigo maligna

Lentigo maligna (melanoma in situ , intraepidermal melanoma, Hutchinson freckle) is an uncommon condition that develops in sun-damaged skin in elderly individuals. Malignant change may occur, with infiltration of the dermis. Histopathology shows intraepidermal proliferation of spindle-shaped atypical melanocytes replacing the basal layer of the epidermis ( Fig. 1.24A ). Clinically lentigo maligna presents as a slowly expanding pigmented macule with an irregular border ( Fig. 1.24B ). Treatment is usually by excision. Nodular thickening and areas of irregular pig­mentation are highly suggestive of malignant transformation ( Fig. 1.24C ).

Lentigo maligna of the eyelid. (A) Histopathology shows melanoma cells proliferating within the basal layers of the epidermis; (B) early lentigo maligna; (C) melanoma arising from lentigo maligna

(Courtesy of L Horton – fig. A; S Delva – fig. C)

Melanoma

Histopathology shows large atypical melanocytes invading the dermis ( Fig. 1.25A ). Superficial spreading melanoma is characterized by a plaque with an irregular outline and variable pigmentation ( Fig. 1.25B ). Nodular melanoma is typically a blue – black nodule surrounded by normal skin ( Fig. 1.25C ). Treatment is usually by wide excision and may include local lymph node removal. Radiotherapy, chemotherapy, biological and ‘targeted’ therapy may also be used, generally as adjuvants.

Melanoma. (A) Histopathology shows melanoma cells within the dermis; (B) superficial spreading melanoma; (C) nodular melanoma

(Courtesy of J Harry – fig. A)