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Uveoscleritis after excessive neodymium:YAG laser posterior capsulotomy Carl P. Herbort, M.D. ABSTRACT A 66-year-old woman developed severe and recurrent scleritis and uveitis after neodymium:YAG capsulotomy performed 18 months after cataract extraction. Four cracks on the intraocular lens and plastic splinters in the vitreous indicated that excessive laser energy had been used. Inflammation was treated successfully only when a combination of dexamethasone acetate 0.1% drops (Maxidex®), drops of diclofenac sodium 0.1% (Voltaren® Ophtha), and systemic diclofenac sodium (Voltaren®) was used. Inflammation might be explained by chronic irritation of the ciliary body by a displaced haptic or by an immune reaction triggered by damage to the ciliary body at the time of excessive posterior capsulotomy. Key Words: neodymium:YAG laser posterior capsulotomy, nonsteroidal anti- inflammatory drugs, scleritis, uveitis Neodymium:YAG (Nd:YAG) laser posterior capsu- lotomy is a safe procedure causing minimal inflam- mation. 1 Acute intraocular pressure rise, occurring in 15% to 7 3% of eyes, is related to the generation of particles in the anterior chamber and can be prevented by adequate antihypertensive therapy. 1 2 The incidence of severe complications such as retinal detachment and cystoid macular edema (CME) is only 0.5% to 2.0%, yet complications from excessive intraocular laser energy are always possible. This is, to my knowledge, the first description of uveoscleritis as a complication of poste- rior capsulotomy. CASE REPORT A 66-year-old woman was referred to our uveitis clinic for anterior nongranulomatous uveitis with scleritis that did not respond to a two-week course of topical (prednisolone acetate 1%, Pred Forte®, six times daily) and periocular steroids (two injections of dexamethasone phosphate, 5 mg). Her right cat- aract had been removed by phacoemulsification with posterior chamber intraocular lens (IOL) implantation 18 months ear- lier and an Nd: Y AG laser posterior capsulotomy had been per- formed ten days before the onset of inflammation. At presentation, the patient complained of a painful eye with marked loss of vision. Her visual acuity was less than 20/200. There was a diffuse thickening and injection of the conjunctiva, episclera, and sclera and a marked nongranulo- matous anterior chamber. flare was 400 ± 25 photonsjmsec (ph/ms) and cell concentration was 34 ± 5 cells/0.075 mm 3 as measured with the Kowa FC-1000 laser flare-cell meter (cor- responding to 4+ flare and 4+ cells by slitlamp examination). Intraocular pressure was 12 mm Hg. The IOL was not well visualized behind the turbid anterior chamber. The fundus bad a normal red reflex but no details could be seen. No CME was seen with fluorescein angioscopy. Examination of the left pba- kic eye was unremarkable. Because an anaerobic infection was suspected and the in- flammation was mostly anterior, an anterior chamber tap was performed for aerobic and anaerobic cultures, which were observed for 20 days but remained negative. Investigations for a systemic inflammatory or autoimmune disease were nega- tive. Antinuclear antibodies, rheumatoid factor, erythrocyte sedimentation rate, lysozyme, and angiotensin converting en- zyme were all negative or within normal limits. Serology for syphilis was negative. Titers for cytomegalovirus, herpes sim- plex virus, Epstein-Barr virus, and varicella-zoster virus were not elevated. · The patient was treated with systemic diclofenac sodium (Voltaren®), a nonsteroidal anti-inflammatory drug (NSAID); topical diclofenac sodium 0.1% (Voltaren® Ophtha); drops of dexamethasone acetate 0.1% (Maxidex®); and mydriatic drops, which relieved the ocular pain and progressively cleared the anterior chamber. A better view showed that the IOL's posterior surface was marked by four impacts and splinters of plastic were floating in the vitreous adjacent to the lens, indicating that excessive laser energy had been used (Figure 1 ). Also, the IOL's haptics were in an in-and-out-of-the-bag position. There was no clinical evidence of delayed-onset chronic postoperative endophthalmitis. In particular, no white plaques Reprint requests to Carl P. Herbort, M.D., Hopital Jules Gonin, Department of Ophthalmology, University of Lausanne, 15 Ave de France, CH-1 004 Lausanne, Switzerland. 80 J CATARACf REFRACf SURG-VOL 20, JANUARY 1994

Uveoscleritis after excessive neodymium:YAG laser posterior capsulotomy

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Uveoscleritis after excessive neodymium:YAG laser posterior capsulotomy

Carl P. Herbort, M.D.

ABSTRACT A 66-year-old woman developed severe and recurrent scleritis and uveitis after neodymium:YAG capsulotomy performed 18 months after cataract extraction. Four cracks on the intraocular lens and plastic splinters in the vitreous indicated that excessive laser energy had been used. Inflammation was treated successfully only when a combination of dexamethasone acetate 0.1% drops (Maxidex®), drops of diclofenac sodium 0.1% (Voltaren® Ophtha), and systemic diclofenac sodium (Voltaren®) was used. Inflammation might be explained by chronic irritation of the ciliary body by a displaced haptic or by an immune reaction triggered by damage to the ciliary body at the time of excessive posterior capsulotomy.

Key Words: neodymium:YAG laser posterior capsulotomy, nonsteroidal anti­inflammatory drugs, scleritis, uveitis

Neodymium:YAG (Nd:YAG) laser posterior capsu­lotomy is a safe procedure causing minimal inflam­mation. 1 Acute intraocular pressure rise, occurring in 15% to 7 3% of eyes, is related to the generation of particles in the anterior chamber and can be prevented by adequate antihypertensive therapy. 1•2 The incidence of severe complications such as retinal detachment and cystoid macular edema (CME) is only 0.5% to 2.0%, yet complications from excessive intraocular laser energy are always possible. This is, to my knowledge, the first description of uveoscleritis as a complication of poste­rior capsulotomy.

CASE REPORT

A 66-year-old woman was referred to our uveitis clinic for anterior nongranulomatous uveitis with scleritis that did not respond to a two-week course of topical (prednisolone acetate 1%, Pred Forte®, six times daily) and periocular steroids (two injections of dexamethasone phosphate, 5 mg). Her right cat­aract had been removed by phacoemulsification with posterior chamber intraocular lens (IOL) implantation 18 months ear­lier and an Nd: Y AG laser posterior caps ulotomy had been per­formed ten days before the onset of inflammation.

At presentation, the patient complained of a painful eye with marked loss of vision. Her visual acuity was less than 20/200. There was a diffuse thickening and injection of the conjunctiva, episclera, and sclera and a marked nongranulo­matous anterior chamber. flare was 400 ± 25 photonsjmsec (ph/ms) and cell concentration was 34 ± 5 cells/0.075 mm3 as

measured with the Kowa FC-1000 laser flare-cell meter (cor­responding to 4+ flare and 4+ cells by slitlamp examination). Intraocular pressure was 12 mm Hg. The IOL was not well visualized behind the turbid anterior chamber. The fundus bad a normal red reflex but no details could be seen. No CME was seen with fluorescein angioscopy. Examination of the left pba­kic eye was unremarkable.

Because an anaerobic infection was suspected and the in­flammation was mostly anterior, an anterior chamber tap was performed for aerobic and anaerobic cultures, which were observed for 20 days but remained negative. Investigations for a systemic inflammatory or autoimmune disease were nega­tive. Antinuclear antibodies, rheumatoid factor, erythrocyte sedimentation rate, lysozyme, and angiotensin converting en­zyme were all negative or within normal limits. Serology for syphilis was negative. Titers for cytomegalovirus, herpes sim­plex virus, Epstein-Barr virus, and varicella-zoster virus were not elevated. ·

The patient was treated with systemic diclofenac sodium (Voltaren®), a nonsteroidal anti-inflammatory drug (NSAID); topical diclofenac sodium 0.1% (Voltaren® Ophtha); drops of dexamethasone acetate 0.1% (Maxidex®); and mydriatic drops, which relieved the ocular pain and progressively cleared the anterior chamber.

A better view showed that the IOL's posterior surface was marked by four impacts and splinters of plastic were floating in the vitreous adjacent to the lens, indicating that excessive laser energy had been used (Figure 1 ). Also, the IOL's haptics were in an in-and-out-of-the-bag position.

There was no clinical evidence of delayed-onset chronic postoperative endophthalmitis. In particular, no white plaques

Reprint requests to Carl P. Herbort, M.D., Hopital Jules Gonin, Department of Ophthalmology, University of Lausanne, 15 Ave de France, CH-1 004 Lausanne, Switzerland.

80 J CATARACf REFRACf SURG-VOL 20, JANUARY 1994

Fig. 1. (Herbort) Slitlamp view of anterior segment by re­troillumination shows IOL debris in the vitreous (arrows); laser impacts on the IOL superiorly.

were seen on the remaining posterior capsule. After one month, inflammation almost completely cleared. Anterior chamber flare dropped to 6.1 ± 0.8 ph/ms (normal value = 3 ph/ms to 5 ph/ms) and there were no cells. Visual acuity returned to 20/20, and no fundus lesions were seen.

During tapering of the medications, the uveoscleritis re­curred twice but promptly responded to increased dosages. After a follow-up of 15 months, inflammation remained under

control with a maintenance therapy ofMaxidex one drop a day and Voltaren Ophtha drops three times a day.

DISCUSSION Although Nd:Y AG laser posterior capsulotomy usu­

ally causes minimal inflammation, excessive intraocular laser energy can cause severe inflammation. In this pa­tient with uveoscleritis, we cannot be absolutely certain that the inflammation was the result of the posterior capsulotomy, although the timing strongly suggests this is the case. Furthermore, immunologic investigations did not show evidence of an underlying systemic in­flammatory or autoimmune disease.

The recurrent inflammation could be explained by damage caused to the ciliary body or to the sulcus by the posterior capsulotomy, which could have triggered an immune reaction or chronic irritation caused by the displacement of an IOL haptic. Only the combination of a NSAID (topical and systemic) with topical corticoste­roids was effective in treating the inflammation.

REFERENCES

1. Altamirano D, Mermoud A, Pittet N, et al. Aqueous hu­mor analysis after Nd:YAG laser capsulotomy with the laser flare-cell meter. J Cataract Refract Surg 1992; 18: 554-558

2. Keates RH, Steinert RF, Puliafito CA, Maxwell SK. Long­term follow-up ofNd:YAG laser posterior capsulotomy. Am Intra-Ocular Implant Soc J 1984; 10: 164-168

J CATARACT REFRACT SURG-VOL 20, JANUARY 1994 81