Basal Cell Carcinoma of the Eyelids

Practicevenkatesh C. Prabhakaran, MS; Mrcophth, Aanchal Gupta, MBBS; Shyamala C. Huilgol, FACD; Dinesh Selva, Franzco


Compr Ophthalmol Update. 2007;8(1):1-14. 

In This Article

Clinical Features

Basal cell carcinomas characteristically arise in body areas exposed to the sun, with 80% developing on the head and neck followed by 15% on the trunk and arms.10 The distribution of BCC may be changing (possibly due to altered sun exposure patterns), with an increased number of trunk tumors described.11 Periocular BCCs most commonly occur on the lower eyelid (43%), followed by the medial canthus (26%), upper eyelid (12%), and lateral canthus (8%).[49] Tumors often present as visible mass lesions, but despite this, they may be present for many months prior to diagnosis. It is important to note that as many as 60% of patients with one BCC may have an unsuspected BCC elsewhere on the face.[50]

Clinically, the classic form is the nodular BCC, which often presents as a pearly papule or nodule with overlying telangectasia and a rolled border (Figure 2A). It enlarges to a dome-shaped tumor and may ulcerate (Figure 2B). The linear variant of BCC is most commonly of nodular subtype histologically, has a predilection for the periocular region, and may have more aggressive behavior.[51]

Clinical appearances of basal cell carcinoma. A: Nodular basal cell carcinoma, showing a pearly nodule with overlying telangiectasia. B: Noduloulcerative basal cell carcinoma demonstrating superficial ulceration. C: Pigmented basal cell carcinoma. Pigmentation of basal cell carcinoma, due to melanin, is of no prognostic significance, but these lesions may be mistaken for melanoma. D: Morpheaform basal cell carcinoma of the lower lid resulting in ectropion. E: Longstanding basal cell carcinoma causing extensive ulceration, soft tissue destruction, and orbital invasion (rodent ulcer). F: Orbital invasion resulting in an immobile lower lid. (Figure 2E is courtesy of Dr. Manel Pasqual, Colombo, Sri Lanka.)

Other forms of BCC include superficial and morpheic. Superficial BCC presents as a scaly erythematous patch or plaque, which can mimic psoriasis, discoid eczema, insitu squamous cell carcinoma, or Bowen disease. It can also mimic other annular dermatoses, such as superficial fungal infections. Superficial BCCs tend to occur on the trunk; they are slow growing and frequently multiple.[52] Both nodular and superficial forms of BCC may contain melanin, imparting a brown, blue, or black color to these lesions. These colored lesions are referred to as pigmented BCCs (Figure 2C). An important clinical subtype is the morpheaform BCC, typically appearing as an indurated, whitish, scar-like plaque with indistinct margins. This subtype has a more aggressive clinical course, and suspicious lesions in high-risk areas should promptly undergo biopsy (Figure 2D). Left untreated over a prolonged period, BCC can lead to extensive soft tissue destruction, which originally gave rise to the term rodent ulcer (Figure 2E).

As BCC can present in a variety of ways, it is not surprising that the diagnosis is clinically missed in 20– 40% of cases.[8] On rare occasions, a lesion manifests tenderness or pain that can be a clue to perineural infiltration. Histological perineural invasion is found in 1–3% of BCCs; it is more common in infiltrating or morpheic tumors[53,54] and is a risk factor for orbital invasion. Signs of orbital invasion include fixation of the tumor mass to bone, limitation of ocular motility, globe displacement, and ptosis44 (Figure 2F) ( Table 3 ). Orbital invasion can also occur along the periosteum without evidence of bony destruction.[8] In addition, the tumor can spread intracranially via the superior orbital fissure and cranial foramina.[55] Intraocular invasion by BCC carcinoma is extremely uncommon[56] and usually occurs in patients who have an advanced tumor with orbital invasion.[57]

Metastasis from BCC is a rare event, with the risk related to the size and depth and, to a lesser extent, the histological subtype of the original tumor.[58,59,60,61] Large, longstanding primary BCC, recurrent BCC, aggressive histology (infiltrating, basosquamous), and perineural invasion are all risk factors for metastasis.[61] It is important to note that 85% of metastases are from primary head and neck BCC, and the incidence is approximately 1.9% for tumors larger than 3 cm in diameter and 50% for tumors larger than 10 cm in diameter.[62] The average age of onset of primary disease is 45 years, and the median interval to metastasis is 9 years.[63] Metastasis is initially to the regional lymph nodes, followed by bone, lung, and liver.64 The prognosis is poor, with mean survival ranging from 8 months to 3.6 years.[64]


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