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We present three rare cases of non-cicatrising upper lid ectropion, seen in two oculoplastic units.
A 92 year old man with progressive dementia presented with a left upper lid ectropion, which could not be repositioned manually. The patient was of normal weight and had no history of obstructive sleep apnoea (OSA), joint laxity, or skin laxity. An injected, oedematous and hypertrophied upper lid tarsus was noted (fig 1A), but no obvious chronic staphylococcal changes. There was no evidence of anterior lamella cicatrisation (fig 1B and 1C). Moderate to severe horizontal laxity of the left upper eyelid and significant laxity of the left lateral canthal tendon (10 mm medial distraction) were noted. On the right side there was an aponeurotic ptosis, with a milder degree of horizontal laxity and lateral canthal tendon laxity (6 mm medial distraction). There was no evidence of enophthalmos. Conservative treatment with an eye shield, lubricants and topical steroids resulted in no improvement and the everted tarsus failed to remain in the correct position when manual repositioning was attempted. The patient underwent a left upper lid lateral full thickness pentagonal wedge resection of 15 mm, and levator aponeurosis reattachment, with no recurrence of ectropion after a 5 month follow up period
A 49 year old man with obesity and OSA, presented with a constant right upper and lower lid ectropion with a severely injected and hypertrophied conjunctiva (fig 2A). He reported usually sleeping on his right side. On examination there was significant horizontal lid laxity of upper and lower lids, as well as of the lateral canthal tendons bilaterally, but no cicatrisation of the anterior lamella. There was marked ptosis on the right and normal levator function. The everted right upper eyelid could not be manually repositioned and there was marked oedema and inflammation of the upper tarsal conjunctiva. He was diagnosed with a floppy eyelid syndrome and right upper and lower lid ectropion, and underwent a right lower lid lateral tarsal sling and a bilateral upper lid lateral full thickness pentagonal wedge resection (10 mm) and blepharoplasty. Several months later, he underwent a right aponeurotic ptosis repair and a second upper lid lateral wedge resection (5 mm) with horizontal tightening for residual upper lid ectropion. No recurrence was noted over a 48 month follow up period (fig 2B).
A 90 year old woman with early senile dementia presented with a right upper eyelid tarsal ectropion which could not be repositioned manually. She denied any history of OSA or eye rubbing and had no significant joint or skin laxity. She was not underweight or overweight for her height and there was no enophthalmos. The everted tarsus was markedly injected and hypertrophied, but no obvious chronic staphylococcal changes were seen and no cicatrisation of the anterior lamella was noted. In addition, she had bilateral medial lower lid ectropions with moderate to severe horizontal lid laxity of upper and lower lids, as well as the lateral canthal tendons (10 mm medial distraction). The patient did not respond to conservative treatment with lubricants and topical steroids, and she underwent right upper lid ectropion repair with a lateral full thickness pentagonal wedge excision (15 mm) and levator aponeurosis reattachment. No recurrence was noted after a 6 month follow up period.
We have described three patients with an unusual presentation of a non-cicatrising constant upper lid ectropion. Correcting the upper lid laxity with a full thickness pentagonal wedge resection and horizontal tightening1 resulted in a good outcome in all patients.
Upper lid ectropion is not common. In newborns, it is usually temporary and responds to conservative measures. Less commonly, it may results from shortage of anterior lamella, as in blepharophimosis syndrome and congenital ichthyosis.2 A recent report found mild degrees of upper lid eversion in a series of patients with multiple endocrine neoplasia type 2B.3 Upper lid ectropion in adults usually results from pathologies affecting the anterior lamella such as chronic sun damage, irradiation, chronic dermatitis, skin infections, ichthyosis, chemical burns, and previous surgery.2 In patients with the floppy eyelid syndrome the spontaneous upper lid eversion usually occurs during night sleep and is easily repositioned manually.4,5 In a recent report, Burkat and Lemke6 described 80 patients with acquired lax eyelid syndrome who were treated with the four eyelid tarsal strip periosteal flap technique. Although all patients had significant horizontal laxity, none of them had spontaneous upper lid eversion. While spontaneous upper eyelid eversion may occur in conditions such as floppy eyelid syndrome or lax eyelid syndrome which induce sufficient lid laxity, manual repositioning is generally possible. In all our patients the ectropion remained constant and could only be corrected surgically. Only patient 2, who was the youngest, was diagnosed with the floppy eyelid syndrome. The other two were older, had no systemic signs of the floppy eyelid syndrome, and the eyelid changes appeared to be age related.
We believe that the marked horizontal laxity was the main causative factor causing upper lid ectropion in our cases, but poor levator muscle function, dehiscence of the aponeurosis, and involutional tarsal changes7,8 may further contribute to tarsal instability and upper lid ectropion. Two of the patients in our series had significant dementia, and frequent eye rubbing resulting in conjunctival forniceal oedema with tarsal conjunctival oedema and inflammation, may have been a factor in preventing repositioning of the everted tarsus. In the case of the patient with floppy eyelid syndrome, traumatic irritation during sleep may have led to sufficient tarsal conjunctival oedema and inflammation to prevent repositioning of the eyelid.
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