Indian Journal of Ophthalmology

BRIEF REPORT
Year
: 2007  |  Volume : 55  |  Issue : 2  |  Page : 144--146

Surgically induced necrotizing scleritis after pterygium surgery


Nikhil S Gokhale1, Rohini Samant2,  
1 Gokhale Eye Hospital and Eyebank, Gokhale Road (S), Dadar West, Mumbai - 400 028, India
2 Dept. of Rheumatology, PD Hinduja National Hospital and Medical Research Center, Veer Savarkar Marg, Mahim, Mumbai - 400 016, India

Correspondence Address:
Nikhil S Gokhale
Gokhale Eye Hospital, Gokhale Road South, Dadar West, Mumbai
India

Abstract

We report a case of surgically induced necrotizing scleritis following pterygium surgery with the bare sclera technique, without the use of adjunctive irradiation or mitomycin C. The patient was successfully treated with systemic immunosuppression.



How to cite this article:
Gokhale NS, Samant R. Surgically induced necrotizing scleritis after pterygium surgery.Indian J Ophthalmol 2007;55:144-146


How to cite this URL:
Gokhale NS, Samant R. Surgically induced necrotizing scleritis after pterygium surgery. Indian J Ophthalmol [serial online] 2007 [cited 2024 Mar 28 ];55:144-146
Available from: https://journals.lww.com/ijo/pages/default.aspx/text.asp?2007/55/2/144/30712


Full Text

Surgically induced necrotizing scleritis (SINS) typically presents postoperatively as a focal area of intense scleral inflammation occurring adjacent to the site of previous scleral or limbal incision.[1],[2] Evidence of connective tissue disease and absence of other causes of scleral necrosis is helpful in making a diagnosis of SINS. Early diagnosis and prompt immunosuppression is required for its successful management. We report a case of SINS following pterygium surgery without the use of adjunctive irradiation or mitomycin C. The patient had serological evidence of connective tissue disease and was successfully treated with systemic immunosuppression.

 Case Report



A 51-year-old female patient presented with severe pain and redness six weeks following pterygium surgery in her left eye. The patient had undergone a pterygium excision with bare sclera technique without any adjunctive mitomycin C or irradiation. Her systemic investigations done preoperatively were normal except for a positive Australia antigen. She had no previous ocular surgery in either eye. Two weeks postoperatively she developed severe pain and redness in the operated eye. She was treated for about a month with tablet diclofenac 50mg twice daily and topical prednisolone 1% eye drops four times a day without much improvement.

At presentation, the scleral bed at the site of the pterygium excision showed significant thinning but was fully epithelized. There was active scleral inflammation adjacent to the site of excision in the upper nasal [Figure 1] and inferior portion [Figure 2] of the sclera. The corneal bed was fully epithelized with no evidence of active corneal melting. Dilated fundus evaluation and 'B' scan ultrasonography did not reveal any evidence of posterior scleritis. Intraocular pressure was 16 mmHg by applanation. The other eye was within normal limits. The patient was referred to a rheumatologist and gastroenterologist for further evaluation and immunosuppression. Investigations revealed a hemoglobin of 12 gm%, erythrocyte sedimentation rate was 27 mm in first hour (Westergrens), liver function tests were normal, complement 3 (C 3) and complement 4 (C 4) levels were normal, hepatitis B 'e' antigen (HbeAg) and hepatitis B viral (HBV) DNA were negative, chest X-ray PA view was normal and abdominal ultrasonography was normal. Hepatitis B surface antigen (HbsAg) and antinuclear antibody (ANA) tests were positive. Clinically there was no evidence of active liver disease or any systemic collagen vascular disease.

The patient was given pulsed injection of methylprednisolone 1000 mg every day in a slow intravenous infusion for three days. She was given 500 mg cyclophosphamide intravenously on the fourth day and subsequently every month for six months.

There was a rapid improvement in her symptoms and signs after starting treatment. At one month follow-up, inflammation adjacent to the excision site and the upper nasal [Figure 3] and inferior sclera [Figure 4] had subsided. There was evidence of mild patchy scleral thinning in these areas. There was minimal residual scleral inflammation in the temporal area. The inflammation fully subsided in two months. There was no recurrence of inflammation over a period of one year of follow-up.

 Discussion



Surgically induced necrotizing scleritis has been reported to occur after cataract extraction, trabeculectomy, squint surgery, pterygium surgery and surgery for retinal detachment.[1],[2] In SINS there is a variable latent period between surgery and presentation which may vary from one day to 40 years.[1] The area of scleral melt tends to develop adjacent to the surgical wound[1],[2] and may extend to involve the whole anterior segment. These cases may or may not be associated with inflammation.

Autoimmunity or hypersensitivity is now well accepted as an etiological factor in the development of SINS. Immune complexes have been found in and around episcleral vessel walls by immunofluorescence techniques[3] and systemic immunosuppressive regimes have been found to be successful in the treatment of SINS.[1],[2] Clinical or serological markers for connective tissue disorders are present in as many as 62% of cases.[1],[2]

Scleral necrosis and melting may occur after pterygium surgery due to the use of adjunctive irradiation[2],[4],[5] and treatment with mitomycin C.[6] This has been attributed to the prolonged inhibition of wound healing, which can occur with these antiproliferative agents. Excessive cauterization during bare sclera technique is another possible cause of scleral necrosis. Ischemic scleral necrosis can develop with over-cauterization.[7] These etiologies need to be ruled out before we make a diagnosis of SINS.

Medical management of SINS after pterygium surgery has included immunosuppression with oral steroids,[8] methylprednisolone + cyclophosphamide[9] and more recently tacrolimus[10] in a patient not responding to cyclophosphamide and azathioprine. Surgical intervention in the form of tectonic scleral[10] or corneal tissue[11] patch grafts and amniotic membrane grafts[8] has been reported.

Our patient presented with SINS following pterygium surgery. Irradiation, mitomycin C or over-cauterization were not responsible for the scleritis. The inflammation had a latent period of two weeks and was noted adjacent to and away from the surgical site. The patient had serological evidence (positive ANA) but no clinical evidence of connective tissue disease. The patient had a positive Australia antigen but no evidence of active liver disease (normal liver functions) and was at a low risk of infection transmission (negative HbeAg and HBV DNA). There was no response to local steroids and oral nonsteroidal anti-inflammatory therapy, however, the patient showed a good response to immunosuppression with pulsed steroids and cyclophosphamide confirming an underlying immunologic process.

Surgically induced necrotizing scleritis must be considered as a differential diagnosis in patients with scleritis or scleral melting following pterygium surgery, especially if radiation or mitomycin C has not been used. Evidence of connective tissue disease may or may not be found on clinical examination and on laboratory investigations. Early diagnosis and prompt immunosuppression is successful in managing this complication.

 Acknowledgments



We thank Dr. Devendra Desai (Gastroenterologist, P. D. Hinduja National Hospital and Medical Research Center) for helping in the management of this case.

References

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