|Year : 1997 | Volume
| Issue : 1 | Page : 43-45
Surgically induced necrotising scleritis (SINS) - Report of two cases
A Joseph, J Biswas, G Sitalakshmi, L Gopal, SS Badrinath
Medical and Vision Research Foundation, Madras, India
Medical and Vision Research Foundation, Madras
|How to cite this article:|
Joseph A, Biswas J, Sitalakshmi G, Gopal L, Badrinath S S. Surgically induced necrotising scleritis (SINS) - Report of two cases. Indian J Ophthalmol 1997;45:43-5
|How to cite this URL:|
Joseph A, Biswas J, Sitalakshmi G, Gopal L, Badrinath S S. Surgically induced necrotising scleritis (SINS) - Report of two cases. Indian J Ophthalmol [serial online] 1997 [cited 2013 Jun 19];45:43-5. Available from: http://www.ijo.in/text.asp?1997/45/1/43/15025
Surgically induced necrotising scleritis (SINS), is a rare complication of ocular surgery. It was first recognized in 1976 by Arensten et al, who described four patients who developed marginal corneal ulceration after cataract surgery. Lyne and Lloyd-Jones in 1979 described a series of patients without history of scleritis who developed scleral inflammation around a surgical wound. To our knowledge, a single case of this rare entity has been described in the Indian literature. The patient was a 65-year-old diabetic male who developed diffuse scleritis two weeks after suture removal. In addition, he developed exudative retinal detachment and a yellow-white circumscribed fundus mass. Scleritis and retinal detachment resolved after a course of systemic steroids. We report here two well-documented cases of SINS; in both aphakic cases there was no prior history of scleritis and the patients developed necrotising scleritis following suture removal. Both cases showed poor response to systemic steroids and required immunosuppressive agents for control of inflammation.
| Case reports|| |
A 70-year-old male was referred to us in June 1995 with a diagnosis of low grade delayed endophthalmitis in the right eye. He had had an uneventful extracapsular cataract extraction three years earlier with excellent visual recovery. He developed mild irritation of this eye a month and a half before this episode and two loose sutures were removed. Two weeks after the removal of sutures, he developed acute exacerbation of pain, redness and watering with clinical suspicion of mild endophthalmitis. He was treated empirically with broad spectrum topical and systemic antibiotics and a low dose of oral steroids. Additionally, twelve subconjunctival injections of antibiotics were given. There was no growth from the conjunctival swab culture. As the patient showed no improvement, he was treated with antifungal medications-topical pimafucin and oral ketoconazole. The patient had lost his vision in the left eye ten years earlier, following an unsuccessful retinal detachment surgery. He had no history of systemic illness such as diabetes, thyroid disease or rheumatoid arthritis.
On examination his best corrected visual acuity in the right eye was 6/18 N36; the left eye had no perception of light.
Anterior segment examination of the right eye showed a large deep ovoid area of scleral necrosis, with dilated deep episcleral vessels in the upper temporal quadrant, adjoining the line of the surgical scar [Figure - 1]a. There were no cells or flare in the anterior chamber. The left eye was aphakic with a peripheral iridectomy. Intraocular pressure was normal in both eyes. Fundus examination by indirect ophthalmoscopy revealed no abnormalities in the right eye. In the left eye there were multiple vitreous bands with gliotic retina. Clinically he was diagnosed to have low grade endophthalmitis, probably of bacterial origin in the right eye. Scleral necrosis was thought to be due to collagenolytic activity following bacterial infection.
The patient was started on fortified gentamicin and ciprofloxacin eye drops, and oral doxycycline tablet 100 mg twice a day. A scloeral scraping revealed a moderate number of polymorphonuclear cells and occasional gram negative bacteria on microbiological study. No fungal elements were seen. Culture of scleral scraping showed no growth of organisms. On a follow-up after 15 days the patient complained of marked diminution of vision in the right eye. On examination his visual acuity was 6/24. Slit lamp examination revealed few keratic precipitates, aqueous flare (1+) and cells (1+). Fundus showed mild vitreous haze. No exudates were seen in the vitreous cavity. An ultrasound examination revealed shallow peripheral retinal and choroidal detachments. An anterior chamber tap was done to rule out infective endophthalmitis. Direct smear examination revealed many polymorphonuclear cells, and few gram positive bacilli, which were subsequently isolated as Bacillus sphaericus.
As the scleral necrosis continued to progress despite topical and systemic antibiotics, surgically induced necrotising scleritis (SINS) was suspected. Investigations were done to rule out collagen vascular diseases. The erythrocyte sedimentation rate (ESR) and chest X-ray were normal. Rheumatoid factor (RF), antinuclear antibodies (ANA), and anti-neutrophil cytoplasmic antibody (ANCA) were not detected. Post prandial blood sugar, serum immunoglobulin profile and uric acid estimation were within normal limits. The patient was given oral prednisolone 60 mg/day. There was no significant improvement of scleral inflammation after two weeks of treatment and hence immuno-suppressive therapy with oral cyclophosphamide 50 mg twice daily, after baseline haematological investigations (total WBC and platelet counts) was begun. The scleral inflammation showed marked response to treatment. His visual acuity improved to 6/18, N12. The total white cell and platelet counts were monitored weekly. On follow-up after one month of treatment there was complete regression of scleritis [Figure - 1]b. Cyclophosphamide and prednisolone were tapered off. On follow-up after two months his vision reduced again to 6/60, N36. Fundus examination revealed a temporal bullous retinal detachment with macular hole responsible for the visual loss. Patient was advised surgery but refused to undergo the same.
A 65-year-old woman presented in August 1995 with severe pain and diminution of vision in the left eye for twelve days following suture removal. She had undergone an extracapsular cataract extraction in the left eye elsewhere a year ago. She developed mild irritation at the upper limbus and a suture removal was done by her ophthalmologist. Her symptoms exacerbated following this procedure. She had no history of systemic illness. Her visual acuity was 1/60 in the right eye and 2/60 in the left eye. Anterior segment evaluation of the right eye revealed nuclear sclerosis and posterior subcapsular cataract. The left eye showed marked circumciliary congestion, aqueous flare and cells (2+), and a fibrinous membrane on the surface of the intraocular lens. Intraocular pressure was within normal limits in both eyes. Fundus examination by indirect ophthalmoscope was normal in both eyes except for mild vitreous haze in the left eye. She was diagnosed to having low grade endophthalmitis.
She was put on intensive topical ciprofloxacin, steroids and cycloplegics. The patient continued to complain of severe pain, though the anterior chamber reaction decreased. When followed-up after seven days, development of scleral nodules was noticed and a diagnosis of SINS was made [Figure - 2]a. Systemic prednisolone 60 mg/day (1 mg/kg body weight), and oral indomethacin 20 mg twice daily were given. By the next day, the pain greatly reduced. As there was vitreous haze that precluded the view of the fundus, an ultrasound examination was done which revealed a shallow choroidal detachment superiorly. The retina was attached. On successive reviews her visual acuity improved to 6/60. The anterior chamber reaction disappeared, but the scleral inflammation showed no significant improvement. Hence, immunosuppressive therapy with only cyclophosphamide (100 mg/day in two divided doses) was started after baseline white cells and platelet counts. Systemic steroids were tapered off. Investigations revealed a raised ESR and positive anti-nuclear antibody test at 1:256 dilutions by fluorescent antibody technique. The patient was reviewed two weeks later, when the scleritis was markedly reduced. On last follow-up the patient's visual acuity was 6/60. There was almost total resolution of scleritis. Areas of scleral thinning were seen 360° around the limbus [Figure - 2]b.
| Discussion|| |
The aetiology of surgically induced necrotising scleritis has not been established. It is known to occur after cataract extraction, strabismus surgery, trabeculectomy and surgery for retinal detachment. Cataract extraction by a limbal incision has been the most commonly implicated procedure.
SINS has also been associated with multiple surgical procedures, co-existent systemic collagen vascular disease, usage of general anaesthesia, local ischaemia and excessive cautery.
The history should be ascertained and a systemic and laboratory evaluation should be done to rule out any collagen disorder specially rheumatoid arthritis, as these patients are likely to develop post-surgical recalcitrant corneoscleral inflammation. Both patients in this study had no previous history of active collagen vascular disease at the time of presentation. On subsequent investigation, one patient had a raised ESR and positive antinuclear antibody. SINS is now a recognized complication following ocular surgery. It should be included in the differential diagnosis of post-surgical inflammatory disease.
Various treatment modalities advocated in the management of necrotising scleritis include nonsteroidal anti-inflammatory agents (NSAIDs), high doses of systemic steroids, pulsed intravenous steroids, cytotoxic agents and surgery. In a series of 43 patients with SINS, only 3 patients (7%) responded to NSAIDs. Fifteen patients (34.9%) required immunosuppressive therapy alone or in addition to systemic steroids. Systemic steroids are the mainstay of therapy in cases of necrotising scleritis. Treatment is started with a dosage of 1 mg/kg/day and adjusted thereafter according to the response to treatment. Non-steroidal anti-inflammatory agents are also important in controlling the inflammation. However in severe or rapidly progressive cases, cyclophosphamide is the drug of choice, in dose of 2 mg/kg/day in two divided doses. Haematological, urological, and systemic monitoring are mandatory while the patient is in cyclophosphamide therapy.
| References|| |
|1.||Arensten JJ, Christiansen JM, Maumenee AE. Marginal ulceration after intracapsular cataract extraction. Am J Ophthalmol 81:194-197, 1976. |
|2.||Lyne AJ, Lloyd-Jones D. Necrotizing scleritis after ocular surgery. Trans Ophthalmol Soc U.K 99:146-149, 1979. |
|3.||Bhattacharjee H, Dutta N and Das K. Clinical course of scleritis induced by cataract surgery: A case report. Ind I Ophthalmol 42:81-83, 1994. |
|4.||O'Donoghue E, Lightman S, Tuft S, Watson P. Surgically induced necrotizing sclerokeratitis (SINS): Precipitating factors and response to treatment. Br J Ophthalmol 76:17-21, 1992. |
|5.||Scott JA, Clearkin LG. Surgically induced diffuse scleritis following cataract surgery. Eye 8:292-297,1994. |
|6.||Hemady R, Tander J, Foster CS. Immunosuppressive drugs in immune and inflammatory ocular disease. Surv Ophthalmol 35:369-381, 1991. |
[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4]