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Year : 2006  |  Volume : 54  |  Issue : 3  |  Page : 199-200

Necrotizing scleritis following diode laser trans-scleral cyclophotocoa- gulation

Medical and Vision Research Foundations, Sankara Nethralaya, 18, College Road, Chennai, Tamil Nadu, India

Correspondence Address:
Sudha K Ganesh
Medical and Vision Research Foundations, Sankara Nethralaya, 18, College Road, Chennai - 600 006
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0301-4738.27074

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We report a case of necrotizing scleritis following diode cyclo-photocoagulation (CPC). A-64-year-old-Asian Indian male presented with pseudophakic corneal decompensation with secondary angle closure glaucoma that was uncontrolled with maximum medical therapy. Trans-scleral diode CPC was performed in the inferior 180-degree section using a standard diode laser with a G-probe. One month later, the patient developed features suggestive of necrotizing scleritis that resolved with systemic steroid therapy. Necrotizing scleritis following diode CPC has been rarely reported. Ophthalmologists should be aware of the possible occurrence of surgically induced nectotizing scleritis following diode CPC.

Keywords: Diode cyclo-photocoagulation, necrotizing scleritis

How to cite this article:
Ganesh SK, Rishi K. Necrotizing scleritis following diode laser trans-scleral cyclophotocoa- gulation. Indian J Ophthalmol 2006;54:199-200

How to cite this URL:
Ganesh SK, Rishi K. Necrotizing scleritis following diode laser trans-scleral cyclophotocoa- gulation. Indian J Ophthalmol [serial online] 2006 [cited 2023 Dec 6];54:199-200. Available from: https://journals.lww.com/ijo/pages/default.aspx/text.asp?2006/54/3/199/27074

Necrotizing scleritis is a serious ocular disease, often associated with systemic autoimmune vasculitis. Surgically induced necrotizing scleritis (SINS) is a destructive form of scleritis reported, following cataract surgery, trabeculectomy, squint surgery, retinal detachment surgery and pterygium excision.[1],[2],[3] It is recognized by a focus of intense scleral inflammation associated with severe ocular pain, that progresses to scleral thinning and even globe perforation due to collagen destruction. Diode cyclo-photocoagulation (CPC) has been used to treat refractory glaucoma which does not respond to medical therapy.[4] We report a case of necrotizing scleritis following diode laser CPC, for the treatment of secondary angle closure glaucoma. Only one such case-report[5] of SINS following diode CPC could be found in the MEDLINE search.

  Case Report Top

A 64-year-old Asian Indian male presented with history of severe ocular pain, redness and photophobia in the right eye for 2 years. He gave a history of cataract surgery with intraocular lens implantation, 4 years ago in the right eye. He had no complaints in the left eye.

On examination, visual acuity in the right eye was counting fingers close to face. Slit lamp examination of the right eye showed pseudophakia and evidence of corneal decompensation. Slit lamp examination of the left eye was normal. The intraocular pressure (IOP) by applanation tonometry in the right eye was 38 mm of Hg. Gonioscopy of the same eye (done prior to corneal decompensation) revealed that the angle was totally closed with peripheral anterior synechiae. Fundus view by an indirect ophthalmoscope was obscured by corneal haze. However, an ultrasound examination of the right eye was found to be normal. As the IOP was not controlled with maximum medical therapy, (Iotim 0.5%, Alphagan, Trusopt eye drops and oral acetazolamide tablets) trans-scleral diode CPC was done in the inferior 180-degree, using a standard diode laser (Iris Medical Instruments, Inc. Mountain View, Ca) with a G-probe. A total of 1800-2000 mW of energy was delivered in 26 shots. The laser energy sub-threshold, was adjusted to an audible 'pop' level with burn duration of 2 seconds. Topical steroids along with oral carbonic anhydrase inhibitors, were advised following the diode laser application.

One month later, the patient presented with complaints of severe eye pain, redness and photophobia. The vision in the affected eye was hand movement close to face. The slit lamp examination of the right eye showed diffuse corneal haze and an area of scleral excavation 3x1 mm in size close to the inferonasal limbus, extending from the 4 to 6 o' clock position [Figure - 1]. The IOP was 9 mm of Hg. Scrapings from the lesion were subjected to microbiological tests, which did not show any microorganism. A diagnosis of necrotizing scleritis following diode CPC was made.

A complete systemic examination revealed that the patient was a chronic smoker and was hypertensive and diabetic for the last 6 years. A laboratory work up for systemic vasculitis (erythrocyte sedimentation rate, rheumatoid factor, antinuclear antibody and anti neutrophilic cytoplasmic antibodies) were done. All were either normal or negative. The patient was treated with systemic steroids 1 mg/kg bodyweight and topical steroids in tapering doses (tapered by 10 mg per week), over six weeks. At the last visit, patient was symptomatically better and the ocular examination showed no signs of active scleritis. He was on a maintenance dosage of oral steroids of 10 mg on alternate days for 3 months and subsequently on 5 mg alternate days for the next 3 months.

  Discussion Top

Scleral inflammation and necrosis are rare sequelae of ocular surgery, with devastating outcome.[3] SINS is four times more common than non-surgically induced necrotizing scleritis.[3] The etiology of SINS is uncertain. The condition may be a result of delayed hypersensitivity reaction, directed against an antigen that is revealed or altered by tissue injury. In a study by Donoghue et al ., 63% of the patients with SINS had an underlying disorder, of which connective tissue disease was the most common. The mean duration of surgery to the appearance of scleritis, was 9 months.[3]

Trans-scleral diode CPC is a known technique for control of IOP in refractory glaucoma.[4] The potential complications reported in this procedure are intraocular hemorrhage, prolonged ocular inflammation, hypotony, phthisis bulbi, visual loss, postoperative pain and need for re-treatment.[4] In addition, conjunctival surface burns and increased peri-limbal conjunctival pigmentation has been reported. Another potential complication is intraocular disruption (pop), that is characterized as an intraocular micro-explosion.[4] Post-operative iridocyclitis is more severe, with an increased number of pops observed.

SINS following diode CPC has been reported by Shen et al[5] in a 23-year-old woman who developed SINS, 10 months after diode CPC application in 360 degrees in the first sitting and the inferior 180 degrees in the second sitting, with an energy of 2000 mW for the treatment of neovascular glaucoma secondary to central retinal vein occlusion. In our case, a 64-year-old man developed SINS, just one month after diode CPC that was done to control the refractory secondary angle closure glaucoma. We had applied the laser only in the inferior 180 degrees with energy of 1800-2000 mW in 26 shots and adjusted to an audible pop sub-threshold level with a burn duration of 2 seconds. The similarities between our case, as well as the study by Shen et al ., was that the area of SINS corresponded to a site of diode CPC and in both the cases, inflammation resolved with a high dose of systemic steroids.

Diode CPC can cause destruction of pars plicata and sclera.[7] Damage to the pars plicata may activate the complement pathway, with release of chemotactic factors. The necrotizing scleritis noticed in our patient could be due to a direct tissue insult, combined with a type 3 hypersensitivity reaction caused by autoimmunity. In our patient, all the hematological tests, as well as tests for connective tissue disorders were negative. The only systemic association was hypertension and diabetes mellitus.

The ophthalmologist should remain alert about the possible occurrence of SINS following diode CPC. The time interval between diode CPC application and SINS may vary from one month to several months. Literature[1],[3],[5],[6] search reveals that SINS might be the first manifestation of a potentially lethal systemic autoimmune vasculitic disease.

  References Top

De la Maza MS, Foster S. Necrotising scleritis after ocular surgery: A clinicopathologic study. Ophthalmology 1991;98: 1720-6.  Back to cited text no. 1
Watson P, Hazleman BL, Pavesio CE, Green WR, Clinical presentation of Scleritis and episcleritis. In : Watson P, The Sclera and Systemic Disorders 2nd ed. 2004. p. 72-7.  Back to cited text no. 2
Donoghue EO, Lightman S, Tuft S, Watson P, Surgically induced necrotising sclerokeratitis (SINS): Precipitating factors and response to treatment. Br J Ophthalmol 1992;76:17-21.  Back to cited text no. 3
Pastor SA, Singh K, David A, Lee DA, Juzych MS, Lin SC, et al . Cyclophotocoagulation: A report by the American Academy of Ophthalmology. Ophthalmology 2001;108:2130-8.  Back to cited text no. 4
Shen SY, Lai JS, Dennis Lam SC, Necrotising Scleritis following diode laser trans-scleral cyclophotocoagulation. Ophthalmic Surg Lasers Imaging 2004;35:251-3.  Back to cited text no. 5
Sridhar MS, Bansal AK, Rao GN. Surgically induced necrotizing scleritis after pterygium excision and conjunctival autograft. Cornea 2002;21:305-7.   Back to cited text no. 6
McKelvie PA, Walland MJ. Pathology of cyclodiode laser: A series of nine enucleated eyes. Br J Ophthalmol 2002;86:381-6.  Back to cited text no. 7


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