ABSTRACT:

Scleritis is a rare, usually painful inflammation of sclera causing scleral melt and exposure of underlying uveal tissue. Although, idiopathic in 50% cases, systemic vasculitides, collagen vascular disorders and autoimmune diseases are well established causes in remaining cases. Diabetes mellitus as an underlying cause of scleritis has not been reported in literature to the best of our knowledge. Microvasculopathy is a well known complication of diabetes mellitus. We are presenting a case report of a painless scleral melting along with involvement of adjacent cornea in a known diabetic patient without any other systemic cause of scleritis.

Keywords:  Scleritis, diabetes mellitus, microvasculopathy.

CASE HISTORY:

 A 48 year old male presented to us with an approximately 5x7 mm well defined  localized area of scleral thinning with prolapsed  underlying uveal tissue involving infero- temporal region of left eye which was painless and gradually progressing for last 2 months. About 2mm of cornea near the limbus was also involved (figure 1). Recorded Snellen’s acuity was 6/6 OD and 6/9 OS.  Ocular examination revealed mild pupillary distortion in the affected eye and moderate non proliferative diabetic retinopathy in both eyes. Gonioscopy was not attempted due to corneal involvement. Ultrasound biomicroscopic examination of the affected eye did not reveal any mass lesion underlying the diseased area. There was no evidence of infection in the vicinity of the lesion. There was no history of ocular trauma, topical medication or any ocular surgery. Patient was a known case of diabetes for past 12 years. No history of any other systemic ailment was there. Haematological investigations revealed ESR- 20 mm at the end of 1^st hour,   TLC and DLC were within normal limits, Rh factor negative, ANA and c-ANCA were negative. Fasting and post prandial blood sugar was 120 and 210 mg % with patient on oral hypoglycemic agents. HbA₁c was 7.3. Renal function tests were within normal limits and no evidence of diabetic nephropathy was there. Patient was advised corneoscleral patch grafting which he deferred.

DISCUSSION:

Systemic cause of scleritis can be identified in only 50 % cases.¹ Scleritis is usually noninfectious and associated with systemic vasculitides, connective tissue disorders and autoimmune diseases. Rheumatoid arthritis is the most common disease associated with scleritis.² Other conditions associated with scleritis are Wegner’s granulomatosis, Polyarteritis nodosa, systemic lupus erthymatosus, relapsing polychondritis, ankylosing spondylitis and inflammatory bowel diseases. Scleritis is also reported after ocular surgery.³ It  is often complicated by involvement of adjacent structures.

All patients with active scleritis require treatment. Treatment options include oral corticosteroids, non steroidal anti-inflammatory agents, intravenous pulsed steroid therapy, cytotoxic agents and surgical reinforcement. Oral corticosteroids are often the first line agents. Refractory and progressive cases require cytotoxic therapy. Cyclophosphamide in a dose of 2mg/kg is a drug of choice.⁴ Surgical reinforcement can be done in patients with severe thinning involving larger area in a quiescent eye. Surgical options include amniotic membrane transplantation, conjunctival flap, scleral and lamellar corneal patch graft. Kim et al reported a series of 16 cases of scleral necrosis in which 13 patients underwent lamellar scleral patch graft along with conjunctival flap and 3 patients underwent only conjunctival flap reinforcement. ⁵ All cases showed excellent surface restoration except one case of graft melting.  

In our case, scleritis was painless and no systemic association was found on investigations except for long standing diabetes mellitus with poor control. A case of fungal scleritis in diabetic patients has been reported in the past.⁶ Diabetes mellitus per se as a cause of scleritis has not been reported to the best of our knowledge.  Considering the fact that diabetes can lead to microvasculopathy, it could be the underlying factor responsible for scleral necrosis in our case.

REFERENCES:

1. Watson PG, Hayreh SS. Scleritis and episcleritis. Br J Ophthalmol. 1976;60:163-91.
2. Afshari NA, Afshari MA, Foster CS. Inflammatory conditions of the eye associated with rheumatic diseases. Curr Rheumatol Rep. 2001;3:453-8.
3. Joseph A, Biswas J ,Sitalakshmi G, Gopal L, Badrinath SS. Surgically induced necrotizing scleritis (SINS)- Report of two cases.Indian J Ophthalmol. 1997;45(1):43-5.
4. Hemady R, Tander J, Foster CS. Immunosuppressive drugs in immune and inflammatory ocular disease. Surv Ophthalmol 35:369-381, 1991.  
5. Kin SY, Chung WS, Hahn DK. Surgical management of scleral necrosis. J Korean Ophthalmol Soc 1995;36(1):7-12.
6. Locher D, Adesina A, Wolf T, et al. Postoperative Rhizopus scleritis in a diabetic man. J Cataract Refract Surg. 1998;24:562-5.