September 25, 2014
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Keratolimbal allograft may be used for ocular surface reconstruction in symblephara treatment

Keratolimbal allograft tissue is an alternative to traditional amniotic membrane or conjunctival grafts.

Thomas John, MD

Thomas John

 

Symblepharon is adhesion of the eyelid palpebral conjunctiva to the bulbar conjunctiva. It may be partial or complete, affecting one or both eyelids, and can cause significant morbidity in affected individuals. Such an adhesion of subepithelial scarring can compromise not only the fornix, but also obliterate the fornix and potentially result in ankyloblepharon, especially if the inflammation is not effectively controlled in a timely fashion. Significant alteration or obliteration of the normally occurring fornix can compromise or eliminate the all-important tear reservoir, as pointed out by Tseng, and secondarily have an adverse effect on the tear meniscus. Without adequate tear spread with each blink, the ocular surface can potentially deteriorate to culminate in irreversible blindness. Hence, symptomatic symblepharon associated with active inflammation needs to be considered a clinically significant finding that requires appropriate management for optimizing outcomes and relieving associated ocular symptoms.

The eyelid is an important and integral component of the mechanisms needed to keep the ocular surface healthy and the cornea transparent. Symblepharon can secondarily affect the eyelid in ways that can limit ocular motility and cause symptoms of diplopia, contribute to incomplete blink and altered tear spread, and result in an unstable tear film; this can lead to an unhealthy, deteriorating ocular surface that can progress to surface keratinization and corneal opacification. Thus, entropion, misdirected lashes, trichiasis, ptosis, lacrimal gland blockage and ankyloblepharon can all be the eyelid effects of uncontrolled, progressive symblepharon. Additionally, anatomic alterations in the fornix can cause difficulty with contact lens wear and interference with intraocular surgery.

While symptoms can vary depending on the etiology of the symblepharon, some of the common symptoms may include redness, foreign body sensation, tearing, burning, lid heaviness, photophobia and diplopia. There may also be blepharospasm, entropion, inadequate lid closure, and ocular motility alterations. Etiologies for symblepharon include, but are not limited to, conjunctival infections (bacterial, viral, chlamydial), allergic conjunctivitis (atopic or vernal conjunctivitis), dry eye syndrome, Stevens-Johnson syndrome, erythema multiforme, toxic epidermal necrolysis, ocular cicatricial pemphigoid, recurrent pterygia and chemical burn. Management of symptomatic symblepharon includes a variety of approaches, some more effective than others. These encompass frequent ocular lubrication using artificial tears and/or ointment, punctal occlusion, bandage contact lens or scleral lens, epilation, symblepharon rings, symblepharon dishes, ProKera (Bio-Tissue), and surgical intervention including symblepharon lysis, amniotic membrane transplantation, use of intraoperative mitomycin C, oral mucosal grafts and conjunctival autografts. It is important to institute systemic immunosuppression in cases of active mucous membrane pemphigoid.

In this column, Dr. Farid describes a new approach to managing symblepharon, especially in those more difficult cases of recurrent symblepharon. Continued clinical monitoring and long-term follow-up are essential for assessment of the overall benefit of this surgical technique.

Thomas “TJ” John, MD
OSN Surgical Maneuvers Editor

Marjan Farid, MD

Marjan Farid

 

There are multiple etiologies in the formation of symblephara, including autoimmune and inflammatory processes as well as trauma, chemical, and thermal injury. In many cases, patients can develop symptomatic motility restriction. Simple excision and removal of scar tissue are often insufficient and frequently result in symblepharon. Such adhesions may result in recurrent or progressive diplopia, restriction of extraocular motility, lagophthalmos or entropion, with all their associated sequelae.

Conventional surgical techniques to address symptomatic symblephara include surface reconstruction with tissue substitutes such as conjunctival or amniotic membrane grafting or synthetic spacers, with or without adjunctive mitomycin C and subconjunctival steroid to decrease the probability of re-scarring. Many of these traditional techniques are insufficient at preventing recurrence.

In cases of symptomatic symblepharon without significant corneal involvement, we describe a novel technique using keratolimbal allograft (KLAL) tissue for ocular surface reconstruction. Edward Holland, MD, has previously described at length the use of KLAL tissue in the surgical treatment of limbal stem cell deficiency by replacing the diseased or deficient cells. This tissue is inherently more robust than conjunctiva or amniotic membrane grafts and therefore provides a superior physical barrier to scar formation. KLAL tissue also provides a supply of ocular surface stem cells that may contribute to a healthier ocular surface in the immediate postoperative period, further deterring symblepharon recurrence.

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Surgical technique

Initial symblepharon excision and meticulous scar tissue removal are performed. In cases in which scar tissue overlies extraocular muscles, the scar tissue need to be identified and hooked to minimize inadvertent excision of muscle tissue. Surrounding granulation tissue should be carefully removed to result in a freely mobile globe, confirmed by forced ductions.

Ocular surface reconstruction using KLAL for the treatment of recurrent symblephara. Postoperative day 1.

Figure 1. Ocular surface reconstruction using KLAL for the treatment of recurrent symblephara. Postoperative day 1.

Source: Farid M

Ocular surface reconstruction using KLAL for the treatment of recurrent symblephara. Three months after surgery.
Ocular surface reconstruction using KLAL for the treatment of recurrent symblephara. Three months after surgery.

Figures 2 and 3. Ocular surface reconstruction using KLAL for the treatment of recurrent symblephara. Three months after surgery.

 

The donor corneal tissue should be ordered from the eye bank with a large rim and conjunctiva attached. A 7.5-mm trephine is used to excise a central corneal button, which is discarded. The remaining keratolimbal tissue is then segmented into two to three equal sections. Each section is trimmed and thinned by 50% using a crescent blade. The corneal end is further tapered to minimize a step-off when placed onto the ocular surface. Two cornea donors may need to be used in cases of extensive scarring. The sections are then positioned concentrically in correct anatomic orientation to entirely cover the area of exposed sclera and deep into the forniceal origin of the symblepharon. Each segment is sutured to the globe without any gaps between segments.

Postoperative steroids and antibiotics are used. Topical steroids are maintained for several months. To date, five eyes with recurrent symblepharon resulting in restrictive diplopia that had failed previously stated surgical therapies have been treated with this technique with no evidence of recurrence (follow-up: 4 to 18 months) and complete resolution of the diplopia with fully restored range of extraocular motility.

Keratolimbal allograft tissue is a robust tissue alternative to traditional amniotic membrane or conjunctival grafts. Ocular surface reconstruction with KLAL may be an effective new procedure in the treatment of symblepharon.

Figures 1 through 3 show the postop day 1 and month 3 results of a 62-year-old woman who had symblepharon formation from the lateral canthus to the temporal limbus after a lateral canthoplasty and lid tightening procedure. She had undergone two previous attempts at symblepharon excision, including amniotic membrane grafting with MMC. There was significant recurrence of the symblepharon despite these attempts. The extent of her symblepharon scarring was causing diplopia in primary gaze and severe restriction in adduction due to tethering of the globe.

References:

Dua HS, et al. Surv Ophthalmol. 2000;doi:10.1016/S0039-6257(00)00109-0.
John T, et al. Ophthalmology. 2002;doi:10.1016/S0161-6420(01)00900-9.
Kheirkhah A, et al. Am J Ophthalmol. 2008;doi:10.1016/j.ajo.2008.03.028.
Kheirkhah A, et al. Cornea. 2013;doi:10.1097/ICO.0b013e318247983d.
Ramaesh K, et al. Eur J Ophthalmol. 2003;13(6):515-524.
Tseng SC, et al. Ophthalmology. 2005;doi:10.1016/j.ophtha.2004.11.041.

For more information:

Marjan Farid, MD, is associate professor of ophthalmology and Director of Cornea, Cataract, and Refractive Surgery, Gavin Herbert Eye Institute. She can be reached at University of California, Irvine, 850 Health Sciences Road, Mail Code: 4375, Irvine, CA 92697; 949-824-0327; email: mfarid@uci.edu.
Edited by Thomas “TJ” John, MD, a clinical associate professor at Loyola University at Chicago and in private practice in Oak Brook, Tinley Park and Oak Lawn, Ill. He can be reached at 708-429-2223; fax: 708-429-2226; email: tjcornea@gmail.com.

Disclosure: Farid has no relevant financial disclosures. John is a consultant for, equity owner in and on the speaker bureau of Bio-Tissue.