Eyelid retraction has numerous causes. Most notably eyelid retraction is caused by thyroid eye disease (TED), trauma, and postsurgical changes. The upper eyelid margin is typically measured at 3.5 to 4.5 mm above the center of the cornea. The lower eyelid margin is typically situated at the inferior border of the limbus. Eyelid retraction is a condition in which the upper eyelid margin is displaced superiorly or the lower eyelid margin is displaced inferiorly. Eyelid retraction may result in exposure keratopathy and disturbing ocular symptoms, including blurred vision, photophobia, foreign body sensation, burning, and reactive tearing. Eyelid retraction in TED is thought to be due to a combination of inflammation, fibrosis, and adrenergic stimulation of the eyelid retractors. Proptosis can also contribute to eyelid retraction. In the upper eyelid, factors responsible for eyelid retraction include (1) inflammation and fibrosis of the levator and Müller’s muscles, (2) adrenergic stimulation of Müller’s muscle, and (3) inflammation and fibrosis of the inferior rectus muscle, causing hypodeviation of the globe and compensatory overaction of the superior rectus–levator complex. In the lower eyelid, factors responsible for eyelid retraction include (1) inflammation and fibrosis of the inferior rectus muscle with consequent traction on its anterior extension, the capsulopalpebral fascia, which is the main lower lid retractor, and (2) adrenergic stimulation of the smooth muscle fibers within the lower lid retractor complex. A combination of eyelid retraction and proptosis in TED may result in ocular exposure with symptoms of ocular irritation, an undesirable cosmetic appearance, corneal erosion and infection, or (rarely) globe luxation. Mild exposure problems can be managed with topical lubricants. Guanethidine, a topical sympatholytic agent, is of limited usefulness in the management of eyelid retraction due to its variable efficacy and frequent ocular side effects, including irritation, hyperemia, photophobia, pain, edema, burning sensation, and punctate keratitis. It may be more tolerable if used in lower concentrations. Exposure problems in the inflammatory phase of the condition present a special challenge as surgical correction of eyelid retraction is best performed in the pos-tinflammatory, stable phase. Several reports have described using Botulinum toxin injections, 2.5 to 15 U, either subconjunctivally or percutaneously, just above the superior border of the tarsus.
A 12-year-old boy and 63-year-old woman were incidentally found to have a solitary, well-defined, raised, ovoid lesion involving the inferomedial palpebral conjunctiva. Both lesions were separate from the lacrimal caruncle with normal conjunctiva surrounding the lesions. Excisional biopsies were consistent with caruncular tissue. In the English literature, supernumerary lacrimal caruncle has only been previously described in adults despite the congenital nature of the lesion.
To evaluate the efficacy of graded full-thickness anterior blepharotomy for upper eyelid retraction of various causes not associated with Graves eye disease.Twenty-one eyelids of 18 patients with upper eyelid retraction not caused by Graves eye disease were treated with graded full-thickness anterior blepharotomy. Preoperative and postoperative symptoms, midpupil to upper eyelid distance, lagophthalmos, and superficial punctuate keratopathy were evaluated.Upper eyelid retraction was due to facial nerve palsy in 4 patients (22%), overcorrected ptosis in 5 patients (28%), and cicatrix after trauma in 6 patients (33%). One patient each (6% each) had retraction from graft-versus-host disease, after blepharoplasty, and after orbicularis oculi myectomy for blepharospasm. At a mean of 10 months follow-up, presenting symptoms resolved or improved in 17 patients (94%) and remained unchanged in 1 patient (6%). Midpupil to upper eyelid distance, lagophthalmos, and superficial punctuate keratopathy all improved significantly (all p < 0.001). No surgical complications occurred.Graded full-thickness anterior blepharotomy is a safe, effective, and rapid technique for patients with symptomatic upper eyelid retraction due to etiologies other than Graves eye disease. This technique improves symptoms and signs of ocular exposure while addressing relative upper eyelid height symmetry and contour.
In Brief Purpose: To assess the efficacy of a comprehensive technique for correction of severe punctal and medial lower eyelid ectropion and lower eyelid retraction associated with medial canthal ligament (MCL) laxity. Methods: A comprehensive technique that plicates the anterior and posterior crura of the MCL was performed on 8 eyelids of 6 patients with punctal ectropion and MCL laxity. Preoperative and postoperative symptoms, punctal ectropion, medial lower eyelid ectropion, lower eyelid retraction, lagophthalmos, and exposure keratopathy were evaluated. Results: At an average of 13 months (range, 8–17 months), preoperative symptoms of epiphora and discomfort improved or resolved in all eyes. Punctal ectropion improved in all eyes and completely resolved in 75% of eyes. Medial lower eyelid ectropion was corrected in all eyes, when present. Lower eyelid retraction, lagophthalmos, and exposure keratopathy improved in all eyes. In 1 case, edema of the caruncle and semilunar fold persisted for 6 months. Conclusions: Combined anterior and transcaruncular MCL plication is an effective and safe procedure for addressing severe punctal and medial lower eyelid ectropion that accompanies MCL laxity and is difficult to correct by other methods. This procedure provides stable, 3-dimensional support to the medial lower eyelid and punctum. The authors present a novel technique that provides comprehensive, sturdy support of the medial canthal ligament to correct severe punctal and medial lower eyelid ectropion and lower eyelid retraction.
This is a case of a 67-year-old female with a history of Graves’ disease and associated thyroid eye disease who presented to the emergency room after falling and hitting her head. Subsequently, she noted periorbital air on the left side when blowing her nose. A CT scan in the emergency room revealed a left orbital floor fracture and decompression of the left orbit. While nonsurgical orbital decompression in the setting of Graves’ eye disease has been reported in several instances, spontaneous ethmoid bone remodeling or fracture has been the most cited mechanism, with rarer instances of true spontaneous orbital floor fracture. Furthermore, there exist only two known case reports of traumatic orbital floor fractures with subsequent orbital decompression in the setting of thyroid eye disease. In only one of the two known cases, therapeutic effect was established. However, no significant follow-up period was noted. This case represents a rare traumatic orbital floor fracture resulting in orbital decompression with demonstrably improved exophthalmos. It is the first to include definitive follow-up both before and after operative management of the contralateral orbit.
