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.

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.

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).

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.

(Courtesy of H Frank)