Description

A 60-year-old man presented with a 2-year history of gradually worsening ptosis affecting his left upper lid. Nine years ago he had undergone excision of a left acoustic neuroma; this resulted in a left-sided facial palsy, which was partially treated with a facial nerve graft. Despite this, his left eyelid closure remained poor and within 1 year he developed exposure keratopathy. An upper lid gold weight implant was then inserted to improve the lid closure.

At presentation, the eye examination revealed a 3.5 mm left-sided ptosis, pupils were equal and reactive to light and the ocular motility was normal. Bilaterally upper lid dermatochalasis was noted, additionally, a firm 6 mm×20 mm protuberant mass was noted beneath the skin overlying the left upper lid (figure 1).

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Figure 1

A firm 6 mm×20 mm protruding mass was noted beneath the skin overlying the left upper lid causing a 3.5 mm ptosis.

Blinking and eyelid closure is a function of the orbicularis oculi which is innervated by the temporal and zygomatic branches of the facial nerve. Facial nerve palsies can denervate the orbicularis oculi resulting in lagophthalmos (incomplete lid closure).1 Facial nerve grafts can re-innervate the muscles of the face, although this is often with only partial success.2 Upper eyelid gold weight implantation is one method of improving the lid closure by loading the upper lid with additional weight.3 However, gold weight implant migration can occur resulting in iatrogenic ptosis.4 The management involves removal of the gold weight and reinsertion at a later date if exposure keratopathy recurs.