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ORIGINAL ARTICLE
Year : 1996  |  Volume : 44  |  Issue : 1  |  Page : 23-27

Cyanoacrylate adhesive with conjunctival resection and superficial keratectomy in mooren's ulcer


Sight Savers Cornea Training Centre, L.V.Prasad Eye Institute, Road No.2, Banjara Hills, Hyderabad 500 034, India

Correspondence Address:
Vinay Agrawal
Sight Savers Cornea Training Centre, L.V.Prasad Eye Institute, Road No.2, Banjara Hills, Hyderabad 500 034
India
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Source of Support: None, Conflict of Interest: None


PMID: 8828302

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  Abstract 

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 2020 Jun 4];44:23-7. Available from: http://www.ijo.in/text.asp?1996/44/1/23/24601



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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.[1][2][3] 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,[5] bandage contact lenses,[6] as well as usage of systemic[7],[8] and local[9] immunosuppressive agents. Surgical approaches such as cyanoacrylate tissue adhesive,[10],[11] conjunctival resection,[12] superficial lamellar keratectomy,[13]penetrating keratoplasty,[14] lamellar keratoplasty[14], [15] and keratoepithelioplasty[16] 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 Top


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.

bDiagnostic Criteria

The diagnostic criteria are shown in [Table - 1]. Though Foster[8] 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.

Treatment

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.

Surgical technique

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.

Clinical grading

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 Top


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 Top


Mooren's ulcer is an idiopathic condition characterised by progressive inflammatory thinning of the peripheral cornea.[1],[5]This phenomenon is also described in association with ocular trauma, localised or systemic infections and altered corneal nutritional status.[1],[6],[17]

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.[1],[14] This has been indicated by fluorescent antibody studies,[18],[19]cellular immunity assays,[20][21][22] detection of plasma cells in the adjacent conjunctiva,[20],[23] and increased circulating immune complexes.[24] Murray and Rahi[25] 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,[13],[23] stimulating both humoral and cellular responses. Complement activation then causes the release of chemotactic factors to promote neutrophilic infiltration. Lysosomes from neutrophils,[23]epithelial cells,[12] or corneal stroma,[25] release collagenases that melt the cornea. This process perhaps causes further release of altered corneal antigen, thus perpetuating the process[13] [Figure - 2].

Lysosomes from neutrophils[23] have shown to be a possible source of the collagenase responsible for the corneal stromal destruction. Conjunctival resection[12] 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.[27]

Superficial lamellar keratectomy may aid the removal of corneal antigenic stimulus of the autoimmune process that causes stromal melting.[13] It may also act by reducing activated keratocytes which may be a source of collagenase[26] and polymorphonuclear neutrophils which have already invaded the corneal stroma as part of the pathological process.[22],[23] 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.[35]

Cyanoacrylate tissue adhesives have found various applications in ophthalmology since their first use in the human eye by Webster et al.[28] Its role of tissue adhesive in the management of corneal perforations and descemetoceles is well documented.[31],[32] 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.[10] Though their exact role is not yet defined, polymorphonuclear neutrophils[23] and epithelial cells[26]play 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[10] and prevents epithelial collagenase from reaching the corneal stroma.[30] In addition, it acts as a structural support to the thinned area of the cornea.[10]

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.[10],[31] 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.[11]

In our series, only one eye developed corneal infiltrate at the site of the tissue adhesive, due to subsequent direct trauma. Cavanagh and Gottsch[34] 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 report[32]discounts 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.[33] 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[35].

 
  References Top

1.
Wood TO, Kaufman HE. Mooren's ulcer. Am J Ophthalmol 71:417-22, 1971.  Back to cited text no. 1
    
2.
Tabbara KF, Ostler HB.Mooren's ulcer, In Trevor-Roper P (ed) Proceedings of the 6th Congress of European Ophthalmology, London; Academic Press and Royal Society of Medicine, 1980.  Back to cited text no. 2
    
3.
Hill JC, Potter P. Treatment of Mooren's ulcer with Cyclosporine A: a report of 3 cases. Br J Ophthalmol 71:11-15, 1987.  Back to cited text no. 3
    
4.
Kietzman B. Mooren's ulcer in Nigeria. Am J Ophthalmol 65:679, 1968.  Back to cited text no. 4
    
5.
Brown SI. What is Mooren's ulcer ? Trans Ophthalmol Soc, UK 98:390-392, 1978.  Back to cited text no. 5
    
6.
Joondeph JC, McCarthy WL Jr, Rabb M et al. Mooren's ulcer: two cases occurring after cataract extraction and treated with hydrophilic lens. Ann Ophthalmol 8:187-194, 1976.  Back to cited text no. 6
    
7.
Tauber J, de la Maza MS, Xuan Hoang T et al. An analysis of therapeutic decision making regarding immuno-suppressive chemotherapy for peripheral ulcerative keratitis. Cornea 9:66-73, 1990.  Back to cited text no. 7
    
8.
Foster CS. Systemic immunosuppressive therapy for progressive bilateral Mooren's ulcer. Ophthalmology 92:1436-1439, 1985.  Back to cited text no. 8
    
9.
Zhao JC, Jin XY. Treatment of Mooren's ulcer with cyclosporine A eyedrops. Chin Med J 105:406-409, 1992.  Back to cited text no. 9
    
10.
Fogle JA, Kenyon KR, Foster CS. Tissue adhesive arrests stromal melting in the human cornea. Am J Ophthalmol 89:795-802, 1980.  Back to cited text no. 10
    
11.
Leahey AB, Gottsch JD, Stark WJ. Clinical experience with N-butyl cyanoacrylate (Nexacryl) tissue adhesive. Ophthalmology 100:173-180, 1993.  Back to cited text no. 11
    
12.
Stilma JS. Conjunctival excision or lamellar scleral autograft in 38 Mooren's ulcer in Sierra Leone. Br J Ophthalmol 67:475-478, 1983.  Back to cited text no. 12
    
13.
Martin NF, Stark WJ, Maumenee AE. Treatment of Mooren's and Mooren's like ulcer by lamellar keratectomy: Report of six eyes and literature review. Ophth. Surg.l8:564-569, 1987.  Back to cited text no. 13
    
14.
Brown SI, Mondino BJ. Penetrating keratoplasty in Mooren's ulcer. Am J Ophthalmol 89:255-258, 1980.  Back to cited text no. 14
    
15.
Raizman, MB, de la Maza MS, Foster CS. Tectonic keratoplasty for peripheral ulcerative keratitis. Cornea 10:312-316, 1991.  Back to cited text no. 15
    
16.
Kinoshita AS, Ohashi Y, Ohji M, et al. Long term results of Keratoepithelioplasty in Mooren's ulcer. Ophthalmology 98:438-445, 1991.  Back to cited text no. 16
    
17.
Kuriakose E. Mooren's ulcer: Etiology and treatment. Am J Ophthalmol 55:1064-1069, 1963.  Back to cited text no. 17
    
18.
Schaap OL, FeltKamp TEW, Bregtoart AC. Circulating antibodies to corneal tissue in a patient suffering from Mooren's ulcer (ulcus rodens corneac). Cli Exp Immunol 5:365-370, 1969.  Back to cited text no. 18
    
19.
Van derGaag R, Andillahi H, Stilma JL. Circulating antibodies against corneal epithelium and hookworm in patients with Mooren's ulcer from Sierra Leone. Br J Ophthalmol 67:623, 1983.  Back to cited text no. 19
    
20.
Brown SI, Mondino BJ, Rabin BS. Autoimmune phenomenon in Mooren's ulcer. Am J Ophthalmol 82:835-840, 1976.  Back to cited text no. 20
    
21.
Mondino BJ, Brown SI, Rabin BS. Cellular immunity in Mooren's ulcer. Am J Ophthalmol 85:788-791, 1978.  Back to cited text no. 21
    
22.
Eiferman RA, Hynduik RA, Hensley JT. Limbal immunopathology of Mooren's ulcer. Ann Ophthalmol 10:1203-1206, 1978.  Back to cited text no. 22
    
23.
Foster CS, Kenyon KR, Greier J, et al. The immunopathology of Mooren's ulcer. Am J Ophthalmol 88:149-159, 1979.  Back to cited text no. 23
    
24.
Berkavitz PT, Arentsen JJ, Felberg NT, et al. Presence of circulating immune complexes in patients with peripheral corneal diseases. Arch Ophthalmol 101:242-245, 1983.  Back to cited text no. 24
    
25.
Murray PI, Rahi RHS. Pathogenesis of Mooren's ulcer: some new concepts. Br J Ophthalmol 68:182-187, 1984.  Back to cited text no. 25
    
26.
Gordon JM, Bauer EA, Eison AZ. Collagenase in human cornea. Immunologic localisation. Arch Ophthalmol 98:341-345,1980.  Back to cited text no. 26
    
27.
Robin JB, Schanzlin DJ, Verity SM, et al. Peripheral corneal disorders. Surv Ophthalmol 31:1-36, 1986.  Back to cited text no. 27
    
28.
Webster RA Jr, Slansky HH and Refejo MF. The use of adhesive for the closure of corneal perforations, Report of two lenses Arch Ophthalmol. 80:705-709, 1968.  Back to cited text no. 28
    
29.
Kenyon KR: In discussion on: Hirst LW, Smiddy WE, et al. Corneal perforations. Changing methods of treatment 1960-80. Ophthalmology 89:634-635, 1982.  Back to cited text no. 29
    
30.
Kenyon KR, Berman M, Rose J, et al. Prevention of stromal ulceration in the alkali burned rabbit cornea by glued on contact lens. Evidence for the role of polymorphonuclear leukocytes in collagen degradation. Inv Ophthalmol Vis Sci 18:570-587, 1979.  Back to cited text no. 30
    
31.
Golubovic S, Parunovic A. Cyanoacrylate glue in the treatment of corneal ulcerations. Fortschr Ophthalmol 87:378-381, 1990.  Back to cited text no. 31
    
32.
Weiss JL, William P, Lindstorm RL, et al. The use of tissue adhesive in corneal perforations. Ophthalmology 90:610-615, 1983.  Back to cited text no. 32
    
33.
Eiferman RA, Snyder JW. Antibacterial effect of cyanoacrylate glue. Arch Ophthalmol 101:958-960, 1983.  Back to cited text no. 33
    
34.
Cavanaugh TB, Gottsch JD. Infectious keratitis and cyanoacrylate adhesive. Am J Ophthalmol 111:466-471, 1991.  Back to cited text no. 34
    
35.
Carlson AN, Wilhelmus KR. Giant papillary conjunctivitis associated with cyanoacrylate glue. Am J Ophthalmol 104:437-438, 1987.  Back to cited text no. 35
    


    Figures

  [Figure - 1], [Figure - 2]
 
 
    Tables

  [Table - 1], [Table - 2], [Table - 3]



 

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