|Year : 1996 | Volume
| Issue : 1 | Page : 23-27
Cyanoacrylate adhesive with conjunctival resection and superficial keratectomy in mooren's ulcer
Vinay Agrawal, Aashish Kumar, Virender Sangwan, Gullapalli N Rao
Sight Savers Cornea Training Centre, L.V.Prasad Eye Institute, Road No.2, Banjara Hills, Hyderabad 500 034, India
Sight Savers Cornea Training Centre, L.V.Prasad Eye Institute, Road No.2, Banjara Hills, Hyderabad 500 034
Source of Support: None, Conflict of Interest: None
Seventeen eyes of thirteen patients with Mooren's ulcer were treated with a combination therapy of local and systemic steroids, conjunctival resection, superficial keratectomy and application of cyanoacrylate tissue adhesive. The pathology was classified as acute, subacute and chronic. Ulcers were graded based on the extent of corneal thinning, degree and extent of ulceration, and amount of inflammation. Fourteen eyes (82.4%) healed completely with formation of a vascularised scars, while three eyes (17.6%) failed to respond to treatment and either went into phthisis bulbi or healed with gross tissue distortion. Our study suggests an early intervention of this therapy with cyanoacrylate tissue adhesive application for effective control of Mooren's ulceration.
Keywords: Conjunctival resection - Superficial keratectomy - Mooren′s ulcer -Multicomponent therapy.
|How to cite this article:|
Agrawal V, Kumar A, Sangwan V, Rao GN. Cyanoacrylate adhesive with conjunctival resection and superficial keratectomy in mooren's ulcer. Indian J Ophthalmol 1996;44:23-7
|How to cite this URL:|
Agrawal V, Kumar A, Sangwan V, Rao GN. Cyanoacrylate adhesive with conjunctival resection and superficial keratectomy in mooren's ulcer. Indian J Ophthalmol [serial online] 1996 [cited 2021 Mar 9];44:23-7. Available from: https://www.ijo.in/text.asp?1996/44/1/23/24601
Mooren's ulcer is a peripheral corneal disease characterised by a destructive inflammation of the limbal cornea that progresses centripetally and circumferentially, threatening the clarity of the visual axis and the integrity of the globe. There are two clinical types of Mooren's ulcer. The first type (typical) is usually an unilateral (75%) condition seen in older patients with a protracted course and responds favourably to treatment. The other type (atypical) is a rapidly progressive, bilateral (75%) condition generally encountered in younger men; the outcome following treatment is poor and corneal perforation is seen in 36% of cases. [1,4]
Both medical and surgical forms of treatment have been reported with varying success. Medical therapy includes topical steroids, bandage contact lenses, as well as usage of systemic, and local immunosuppressive agents. Surgical approaches such as cyanoacrylate tissue adhesive,, conjunctival resection, superficial lamellar keratectomy,penetrating keratoplasty, lamellar keratoplasty,  and keratoepithelioplasty have been tried. These methods are effective only at a particular phase in the cascade responsible for the initiation and progression of ulceration.
In our series we have employed limbal conjunctival resection,superficial lamellar keratectomy and application of cyanoacrylate tissue adhesive. We herein report our observations.
| Materials and methods|| |
Thirteen patients with Mooren's ulcer were included in this study. Of these, nine (69.2%) had unilateral and four (30.8%) had bilateral involvement.
The diagnostic criteria are shown in [Table - 1]. Though Foster has laid down well defined criteria for establishing the diagnosis of Mooren's ulcer, three of our patients did not satisfy one criterion. Two patients had a history of cataract extraction and one had a history of trauma. However, their clinical features were suggestive of Mooren's ulcer and a histopathological analysis of the excised conjunctiva further corroborated the diagnosis.
All patients received a combined medical and surgical treatment of a conjunctival resection, superficial lamellar keratectomy and cyanoacrylate tissue adhesive application followed by bandage contact lens insertion. After surgery, local and systemic steroids were instituted and tapered according to response, over a period of one to six months.
Conjuctival resection consisted of isolation and excision of a 2 to 4 mm strip of conjunctiva adjacent to the ulcerated area.Superficial lamellar keratectomy was performed essentially as a debunking procedure. It consisted of excision of the over-hanging edge of the ulcer and scraping of the ulcer bed with a # 15 Bard-Parker blade. Isobutyl cyanoacrylate tissue adhesive (Histoacryl, Germany) was applied in the groove extending 1 mm beyond the demarcated edges of the ulcer and allowed to polymerise. Bandage contact lens was then placed on the cornea (Plano T) after adequate cleaning of the fornices. The fit of the lens was reassessed for adequacy after one hour.
Post operative regimen
Following the surgery, local antibiotic and steroid were instituted. Topical betamethasone 0.1% was used hourly for three to five days and tapered by one half every week. This was maintained on a once-daily basis to control the inflammatory response. Systemic prednisolone was given for one week at a 1 mg/kg/ day, single-dose regimen, and then tapered by 10 mg every eight to ten days. The average duration of treatment 'was four to eight weeks. Once the cornea had healed, the treatment was discontinued. Of the nine unilateral cases, two had a history of cataract extraction and one had antecedent trauma, both possible initiating factors.
The pathology was classified as acute (onset of symptoms within two weeks of presentation) or subacute (onset of symptoms for more than three months prior to presentation). Ulcers were graded on a scale of 0-4 according to the following: (A) extent of corneal thinning (<25% =1; 25-50% =2; 50-75% =3; 75-100% =4); (B) degree and extent of ulceration (the cornea was divided into four quadrants to document the extent of the ulceration); (C) inflammation (degree of injection and/or swelling of the bulbar conjunctiva).
Each eye was also categorised according to the total score obtained by adding the score of each parameter (corneal thinning + quadrants involved + inflammation) as follows: Score 1 to 4 = Group 1, 5 to 8 = Group II and 9 to 12 = Group III. The total score was compared with the mean time taken for complete healing and the end result following treatment.
| Results|| |
Seventeen eyes of thirteen patients were included in the study. The patients included nine men and four women, with a mean age of 47 years (range, 20 to 76 years). Mean duration of the disease prior to examination was 1.6 months (range, 15 days to 7 months) and of treatment was 3.2 months (range, 1 to 6 months). Mean follow up period was 8.2 months (range 2 to 52 months).
Visual acuity at the time of initial examination ranged from 6/6 to light perception. This remained within one line in eight (47.05%) eyes, while a loss of two or more lines occurred in nine (52.9%) eyes. The pathology was acute in three, subacute in six and chronic in four patients. There was no significant difference in outcome detectable among these groups. Four patients with chronic ulcers had a bilateral involvement. In these four patients, eyes with a lower degree of severity (mean total score, 6) had a visual outcome (mean acuity 6/60) better than those with advanced stage of the disease (best visual acuity of only counting fingers close to face).
The mean degree of ulceration was 3 (50 to 75% depth ulceration) and the mean extent was 2.4 quadrants [Figure - 1]. Mean ocular inflammation of the groups was graded as 2.4 [Figure - 1]. The correlation of healing time with severity was as shown in [Table - 2].
Fourteen (82.3%) eyes healed completely with the formation of vascularised scars. Three (17.6%) eyes failed to respond to treatment. All these three eyes had 75 to 100 percent corneal thinning with 3 to 4 quadrant involvement at initial examination. Two of these eyes became phthisical and one developed a flat anterior chamber due to perforation, after which the patient refused any further treatment.
Eight eyes needed reapplication of cyanoacrylate adhesive [Table - 3]. One eye with a history of direct trauma developed peripheral corneal infiltrate. Microbiological evaluation of the infiltrate isolated Pseudomonas aeruginosa. The eye responded well to medical therapy after reapplication of cyanoacrylate tissue adhesive and finally had a best corrected Snellen acuity of 6/9. Three eyes which developed spontaneous perforation had 3 to 4 quadrant involvement with 90 to 95% corneal thinning at the time of initial examination.
| Discussion|| |
Mooren's ulcer is an idiopathic condition characterised by progressive inflammatory thinning of the peripheral cornea.,This phenomenon is also described in association with ocular trauma, localised or systemic infections and altered corneal nutritional status.,,
It is now evident that autoimmune mechanisms are associated with the development of Mooren's ulcer. Damaged corneal tissue or altered corneal antigen may initiate or perpetuate this process., This has been indicated by fluorescent antibody studies,,cellular immunity assays, detection of plasma cells in the adjacent conjunctiva,, and increased circulating immune complexes. Murray and Rahi suggested that immunological abnormalities in Mooren's ulcer may be due to an underlying defect in the immune regulatory system caused by a reduction in the number of suppressor T cells. It could thus be suggested that corneal trauma, infection or systemic disease alter the corneal antigen,, stimulating both humoral and cellular responses. Complement activation then causes the release of chemotactic factors to promote neutrophilic infiltration. Lysosomes from neutrophils,epithelial cells, or corneal stroma, release collagenases that melt the cornea. This process perhaps causes further release of altered corneal antigen, thus perpetuating the process [Figure - 2].
Lysosomes from neutrophils have shown to be a possible source of the collagenase responsible for the corneal stromal destruction. Conjunctival resection has been employed to reduce this load. It is also effective in eliminating the source of immunoglobulins and complement which may mediate the ulcerative process.
Superficial lamellar keratectomy may aid the removal of corneal antigenic stimulus of the autoimmune process that causes stromal melting. It may also act by reducing activated keratocytes which may be a source of collagenase and polymorphonuclear neutrophils which have already invaded the corneal stroma as part of the pathological process., This debunking process, thus complements the role of cyanoacrylate tissue adhesive by blocking an important step in the natural course of Mooren's ulceration [Figure - 2].
The purpose of the bandage contact lens is to cover the cyanoacrylate tissue adhesive and to avoid direct pressure from lids. This prevents complications like irritation and giant papillary conjunctivitis.
Cyanoacrylate tissue adhesives have found various applications in ophthalmology since their first use in the human eye by Webster et al. Its role of tissue adhesive in the management of corneal perforations and descemetoceles is well documented., It is also suggested that it helps arrest the process of stromal melting. [10,30]It has, however, previously been believed that in cases with torrid inflammation (as in Mooren's ulcer), application of cyanoacrylate tissue adhesive may not be effective in arresting the progression of the disease. Though their exact role is not yet defined, polymorphonuclear neutrophils and epithelial cellsplay a significant part in stromal matrix degradation. Cyanoacrylate tissue adhesive application also acts as a barrier to both tear fluid and early regenerating epithelium. This deters the invasion of stroma by polymorphonuclear cells and prevents epithelial collagenase from reaching the corneal stroma. In addition, it acts as a structural support to the thinned area of the cornea.
In our study, cyanoacrylate tissue adhesive has shown promising results in arresting the progression of both, infective and non infective corneal ulcers. We extended its use to all cases of Mooren's ulcer irrespective of the ocular condition at initial examination. In our series none of the seventeen eyes had perforation. Thirteen eyes had Grade 3 to 4 thinning and nine had Grade 3 to 4 inflammation. Fourteen (82.3%) eyes healed completely with the formation of vascularised scars. In our study the healing time ranged from 4 to 24 weeks. The time taken for healing was however, directly related to the degree of severity at the time of initial presentation. Three (17.6%) eyes which failed to respond to treatment were in the advanced stage of ulceration at initial examination. Based on this study, we believe that the application of cyanoacrylate tissue adhesive in the early stage of Mooren's ulcer is an effective therapy in controlling this devastating disease.
It has been earlier suggested that cyanoacrylate tissue adhesive should be in place for four to eight weeks in order to be effective., Our routine was to leave the adhesive in place until it sloughed off spontaneously. In cases needing reapplication of the adhesive, the previous application was easily removed with a fine forceps, as desired by Leahey et al.
In our series, only one eye developed corneal infiltrate at the site of the tissue adhesive, due to subsequent direct trauma. Cavanagh and Gottsch have documented cases of infectious keratitis following cyanoacrylate adhesive application. They concluded that factors like tissue toxicity, microbial colonisation, use of bandage contact lenses and long-term use of prophylactic antibiotics may be responsible for tissue adhesive-related corneal infections. Previous reportdiscounts the role of adhesive as a source of infection. There is evidence to show that isobutyl cyanoacrylate tissue adhesive possesses antibacterial properties, though ineffective against gram negative bacteria. In our patient, the additional factor of trauma is a likely cause of the corneal infection. Such patients would thus need careful monitoring to avoid the disastrous sequelae of infectious keratitis beneath the tissue adhesive.
We conclude that this multicomponent therapy is an effective line of management for Mooren's ulcers. We emphasise that early intervention with this therapy gives the best outcome, as it aids the prompt arrest of ulceration by reducing the immunogenic load, prevents lytic factors from reaching the ulcer, and provides additional tectonic support to the thinned area of the cornea. This enhances tissue healing and breaks the self-perpetuating cycle of ulceration.
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[Figure - 1], [Figure - 2]
[Table - 1], [Table - 2], [Table - 3]