|Year : 1997 | Volume
| Issue : 4 | Page : 238-239
Rheumatoid corneal melting
Gokhale Eye Hospital and Eye Bank, Dadar, Mumbai, India
N S Gokhale
Gokhale Eye Hospital and Eye Bank, Dadar, Mumbai
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Gokhale N S. Rheumatoid corneal melting. Indian J Ophthalmol 1997;45:238-9
Ocular manifestations in rheumatoid arthritis in order of descending frequency include keratoconjunctivitis sicca, scleritis, and sterile corneal ulceration. Sterile corneal ulceration can occur in either the central or peripheral cornea with a paucity of ocular symptoms and may lead to corneal perforation. Systemic immune mediated inflammation, keratoconjunctivitis sicca, and ocular surface infections trigger the process of corneal ulceration. The process of corneal melting is poorly understood. Leukocyte chemotaxis and lysosomal enzymes release collagenases and proteases which destroy corneal collagen and proteoglycans. Ocular melts secondary to ocular surface problems respond to local measures while necrotising immune mediated melts are very difficult to treat.
Successful use of tissue adhesive has been reported in impending or actual corneal perforations. However, its use is restricted to small perforations. Definitive healing without additional intervention has been reported, while other studies have shown very high rate of microbial keratitis and therefore have used it as a tool to delay corneal surgery by 2 months. Lamellar grafts have better structural and visual results than penetrating grafts in corneal melting disorders. Systemic immunosuppression, most commonly cyclophosphamide, has been used for treating rheumatoid ulcerative keratitis.
This is a case report of rheumatoid arthritis induced bilateral immune corneal melting which was treated with cyanoacrylate, pulse steroids, and cyclophosphamide.
| Case|| |
A 52 years female patient with rheumatoid arthritis presented with redness and blurring of vision in both eyes of 15 days duration. On examination, she had visual acuity of 6 / 36 in the right eye and 6 / 60 in the left eye. Lids revealed mild meibomitis, there was ciliary congestion in both eyes, and there were paracentral corneal melts in both eyes with descemetocele formation in the right eye and a small corneal perforation with flat chamber in the left eye. The fundus could not be visualised.
The patient underwent cyanoacrylate tissue adhesive application with bandage contact lens insertion in both eyes. Topically ciprofloxacin 0.3% 6 hourly, homatropine 2% 12 hourly, artificial tears (hydroxypropyl methylcellulose 0.7%) 4 hourly, acetylcysteine 20% 6 hourly, and diclofenac 0.1% 6 hourly were started. Oral doxycycline 100 mg once daily, chloroquine 250 mg once daily, and diclofenac 50 mg twice daily were also started. Intravenous methylprednisolone 500 mg 12 hourly was given for 3 days.
Laboratory investigations revealed low hemoglobin (11.2 gm/dl), high ESR (91 mm at 1 hr by Westergren method), positive rheumatoid factor (160 IU/ml) and positive anti-nuclear antibody (homogeneous pattern in 1:40 dilution).
N-butyl cyanoacrylate was used as tissue adhesive. It has good bond strength with low toxicity. Glue application was done under topical anesthesia with a wire speculum. The necrotic slough and the adjacent epithelium were debrided with a 15 Bard Parker blade. The surface was then dried with Weckcell sponges and the perforation site was identified. Glue was applied with the reverse end of a Weckcell sponge. It was kept gently pressed over the melt/perforation site till polymerisation occured. Microleaks through the layers of the glue were sealed with additional applications. The aim was to have a thin layer of glue sealing and supporting the thinned area. Excess glue was removed with forceps. A few drops of gentamicin were instilled and a piano bandage contact lens inserted. The patient was evaluated 1 hour later for contact lens fit and chamber depth.
On follow-up visits the glue and contact lens was in place and the anterior chamber were deep with no anterior synechiae in both eyes. The ESR dropped to 54 mm/hr. Deep corneal vascularisation was noted one month postoperatively.
Two months postoperatively the patient presented with loose glue and flat chamber in the right eye. On evaluation the right eye had once again developed a melt with a large perforation (2 mm) while the left eye was doing well. The ESR had increased to 64 mm/hr. Repeat application of tissue glue was done. However, the chamber remained flat. Two days later glue application was repeated and the perforation was sucessfully sealed.
It was then decided to immunosuppress the patient. The initial treatment given was IV methylprednisolone 500 mg and IV endoxan 500 mg on the first day, and IV methylprednisolone 500 mg on the second and third days. The maintenance dose was IV endoxan 500 mg every 3 weeks for 6 months.
Hemogram with ESR, liver and renal function tests, and platelet counts were done prior to each dose. The drug was tolerated well and the ESR remained in the mid-30s.
Five months postoperatively the patient presented with loose glue in both eyes. The loose glue was removed in both eyes. The left eye had healed with a vascularised corneal scar and the vision improved to 6/6 and N6 with correction. The right eye revealed a vascularised scar with a central pinpoint perforation. As the chamber became shallow repeat application of glue was done to close the perforation.
One month later the patient again presented with loose glue in the left eye which was removed. A small perforation was still present but the chamber was well formed. A new tight fitting bandage lens was placed. The perforation healed and 2 weeks later the contact lens was removed. Vision in the left eye improved only to 6/60 due to the scar encroaching the visual axis.
The patient was continued on artificial tears, doxycycline, and chloroquine. There has been no recurrence and the eyes have remained quiet over 6 months of follow up. ESR has been in the mid-20s.
| Discussion|| |
Clear guidelines regarding surgical management and the institution of systemic chemotherapy in rheumatoid corneal perforations do not exist. Tissue adhesives are useful in corneal melts with small perforations (upto 2 mm). Larger melts and perforations require sugery. In cases where surgical intervention is planned tissue adhesive application helps delay surgery till immunosuppression is induced. Lamellar grafts have better results than penetrating grafts in corneal melting disorders. Aggresive immunosuppression with pulse steroids, cyclophosphamide, and now cyclosporine, have been shown to improve results in these cases.
This case highlights the successful use of glue in rheumatoid corneal melts. Difficulty in sealing perforations was also encountered. ESR should be monitored regularly and is a good indicator of immune activity. Recurrent melt coincided with an increase in ESR. Pulse steroids induced immunosuppression should be maintained with a immunosuppressive agent such as cyclophosphamide to prevent recurrences. Surgical intervention should be avoided in the presence of uncontrolled immune activity.
| Acknowledgements|| |
I thank Dr. D.S. Gaitonde for referring the patient to me for management; and Drs. Madhukar K. Reddy and B. Rajeev (L.V. Prasad Eye Insitute, Hyderabad), Rajendra Agrawal (Gokhale Eye Hospital), and V.R. Joshi (P.D. Hinduja Hospital, Mumbai) for their help in the care of this patient.
| References|| |
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