Neodymium:YAG laser anterior vitreolysis for Irvine-Gass cystoid macular edema

Neodymium: YAG laser anterior vitreolysis for Irvine-Gass cystoid macular edema Roger F. Steinert, M .D., Paul]. Wasson , M.D.

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Vitreous strands and bands to the wound may cause eccentric pupils, sometimes resulting in optical problems such as pseudophakic edge glare, and can be associated with cystoid macular edema (CME)1 ,2 (the Irvine-Gass syndrome). Iliff first reported visual improvement after surgical section of such vitreous bands. 3 He coined the term "vitreous-tug syndrome," although no evidence that tugging on the vitreous body was responsible for the macular edema was given. Katzen, Fleischman and Trokel 4 ,5 first reported the use of the N d: YAG laser to section vitreous strands. Steinert and Puliafit06 subsequently documented the variability of improvement in fluorescein angiography and vision in a small number of patients. The series reported in this paper expands the small base of reported clinical experience . Several clinical issues are specifically addressed: (1) the overall rate and amount of visual improvement; (2) the differences between patients with large and small degrees of improvement, with particular reference to intraocular lens (IOL) status; (3) the reasons for failure of vitreolysis to improve acuity in some patients; (4) fluorescein angiographic changes after vitreolysis; (5) the time course of visual improvement when it occurs; and (6) complications of Nd:YAG laser vitreolysis.

SUBJECTS AND METHODS Twenty-nine eyes of 28 patients had lysis of strands and bands of vitreous incarcerated in the cataract wound. All treatments were performed by one of the authors (R. F. S.) using a treatment strategy detailed elsewhere .6 In brief, pilocarpine was instilled preoperatively to stretch the vitreous strand maximally. Treatment was performed directly near the limbus, often with the aid of a peripheral button Abraham contact lens (Ocular Instruments, Inc.), with single shots ranging from 3 m] to 6 m], or in cases where the strand was better seen gonioscopically, with a Goldmann three-mirror contact lens and single shots at energies from 5 m] to 9 m]. Total number of pulses ranged from 4 to 225. Four patients required more than one treatment session to lyse all strands fully. Because of the variability in the extent of vitreous band formation in different patients, data on overall mean energy and number of pulses are meaningless. A clinical diagnosis of CME was made independently by two ophthalmologists in all cases. All patients had received topical steroids without improvement in acuity before laser vitreolysis was considered . Twentytwo of the 29 had fluorescein angiographic confirmation of the presence of CME before laser treatment;

From the Department of Ophthalmology, Harvard Medical School, and the Massachusetts Eye & Ear Infirmary, Boston, Massachusetts. Reprint requests to Roger F Steinert, M.D., Cornea Associates, 50 Staniford Street, Boston, Massa chusetts 02114. 304

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seven did not have interpretable fluorescein angiography because of technical difficulties, logistical conflicts, or patient refusal. Since many patients were referred from geographically remote areas, only nine were available for post-treatment fluorescein angiography. All patients had poor vision after the cataract extraction ; the interval between cataract extraction and treatment averaged ten months (range 1 to 42 months). Average follow-up after laser vitreolysis was also ten months (range 3 to 27 months). All patients were treated with topical steroids for up to four months during the post-treatment period until acuity improved. Eight patients who had persistent CME three or more months after laser vitreolysis were treated with oral indomethacin. In three of these patients, oral indomethacin had been used before the YAG vitreolysis without visual acuity improvement. RESULTS The response of visual acuity to the laser treatment is shown in Figure 1. None of the patients had loss of vision after laser vitreolysis. Sixteen of the 29 patients (55%) improved by two or more lines with stable posttreatment acuity. Five (17%) had improved vision by at least two lines but experienced ongoing fluctuation of acuity. Eight (28%) showed less than two lines of improve ment. Table 1 subdivides these groups by IOL status. No patient had a posterior chamber IOL . Improved but fluctuating acuity was associated with the presence of anterior chamber IOLs.

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The time between laser treatment and maximal improvement averaged 3.5 months (range one to seven months). There were no cases of post-treatmen t retinal detachment or persistent elevated intraocular pressure. Five of the eight eyes treated with oral indomethacin after laser vitreolysis improved and remained improved after discontinuation of the indomethacin. The three patients who failed to respond to oral indomethacin prelaser all improved with oral indomethacin postlaser vitreolysis. Three eyes failed to respond to the laser vitreolysis and postlaser indomethacin . The eight patients who did not demonstrate improved acuity showed several types of persistent pathology. Two had progressive maculopathy in addi tion to the CME (one epiretinal membrane , one progressive diabetic maculopathy); two had severe glaucoma with apparent loss of central vision in addition to their CME; two had persistent CME. Two other patients were lost to follow-up without documentation of the basis for persiste nt unimproved acuity. Patients who did not respond to laser vitreolysis had the poorest pretreatmen t visual acuities (20/300 or worse). A statistically S ignificant correlation between duration ofCME and visual improvement could not be established. Table 2 shows the visual acuity and fluorescein angiographic status of the nine patients available for follow-up fluorescein angiography. Improvement in visual acuity generally corresponded to the extent of change in the angiographically demonstrated CME.

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Improved Stable

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Unimproved p ersisten t leakage Other non-cystoid maculopathy present

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DISCUSSION Katzen , Fleischman, and Trokel first reported the use of the Nd:YAG laser as an alternative to conventional surgery for lysis of strands of vitreous to cataract wounds. In their initial series,4 vision improved by variable degrees in all 14 patients. The presence of CME was judged clinically, however, and fluorescein angiography was available for only one eye. In a later report, 5 the series was expanded to 62 eyes, 43 having fluorescein angiographic documentation of CME prelaser and 12 in follow-up. Forty-nine eyes improved by at least two Snellen lines (89%) and 45 eyes (82%) had acuity of 20/40 or better at a follow-up of one to 14 months compared to only two eyes prelaser. All patients were said to have some degree of improvement in acuity after treatment. Steinert and Puliafit0 6 described the results of anterior vitreolysis in 14 patients with angiographically proven CME; follow-up fluorescein evaluation was available in seven cases. Vision improved in 12 cases. In the seven cases with fluorescein angiography followup, three patients had complete resolution ofCME and visual recovery better than 20/40, three patients had a reduction in CME with partial improvement in acuity, and one patient had no change in CME or improvement in vision. Because of the unpredictable natural history of aphakic CME, with erratic response to anti-inflammatory agents and frequent spontaneous improvement, 7,8 only a large, prospective randomized series could unequivocally prove the efficacy of Nd:YAG laser anterior vitreolysis for CME treatment. Spontaneous improvement of CME associated with vitreous to the wound has not been reported in a large series, however, and may be less common than reported in studies of aphakic CME. The previously reported laser vitreolysis series 4,5.6 strongly suggest a therapeutic effect because of the frequency and temporal relationship of improvement to the laser treatment. Seventy-two percent (72%) of the patients in this series who were treated by Nd:YAG laser anterior vitreolysis for CME experienced improved acuity in the months following treatment; 55% had dramatic and stable improvement . At least half of those who failed to improve had coexisting pathology. These results support prior series demonstrating apparent efficacy of this technique. Notably, no patients experienced any complications. In our series, the patients who showed most improvement were those whose pretreatment visual acuities were 20/100 or better. Because spontaneous improvement in aphakic CME is known to occur, a randomized prospective study with medically treated controls is ideal. The perceived low risk of Nd:YAG laser vitreolysis (confirmed in this study) com bined with the increasing chance of irreversible retinal damage from ongoing CME prevented 306

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implementation of such a controlled trial. Each patient had failed to improve with topical steroids before the laser vitreolysis, with duration of CME averaging ten months (range 1 to 42 months). Improvement of more than two Snellen lines occurred in 72% of cases within one to seven months (mean 3.5 months), which is unlikely to be spontaneous. Cystoid macular edema after cataract surgery remains a poorly understood phenomenon . Inflammation of the anterior and posterior uvea, mediated by prostaglandins, speCifically PGE 2, appears to be the basis of manv cases. 9 - 12 TI;e specific mechanism ofCME in association with vitreous to the wound is unknown; because many cases have a posterior vitreous detachment, the hypothesis of direct traction on the macula is no longer widely accepted. 7,8,13-16 We adhere to the hypothesis that a strand of vitreous incarcerated in the wound causes chronic irritation of the iris, resulting in the inflammatory response, including CME. A study of iris fluorescein angiography showed that 100% of cases with CME and vitreous incarceration demonstrated fluorescein leakage from the pupillary margin. 17 This hypothesis is also consistent with the recognized higher incidence of CME with certain anterior chamber IOLs and especially with iris fixated IOLs.18 All five cases of fluctuating vision after vitreolysis had anterior chamber IOLs, which may have contributed to the ongoing CME. In a major prospective randomized multicenter study, Fung et aP6 have demonstrated the efficacy of vitrectomy in treating CME associated with vitreous incarceration in the cataract wound. Increasing favorable experience with N d: YAG laser vitreolysis suggests that it is the relief of traction to the wound , rather than the removal of th e anterior vitreous, which is the major therapeutic factor. In cases of extensive anterior vitreous adhesion to the anterior segment, including anterior and posterior iris, N d: YAG laser vitreolysis would be inadequate and vitrectomy would be required, REFERENCES 1. Irvine SR: A newly defined vitreous syndrome follOWing cataract surgery; interpreted according to recent concepts of the structure of the vitreous. Am ] Ophthalmol 36:.599-619, 19.53 2. Gass .TOM , Norton EWO: Cystoid macular edema and papilledema following cataract extraction ; a flu orescein fun doscopic and angiographic study. Arch Ophtlwlmol 76:646661, 1966 3. Iliff CE: Treatment of the vitreous-tug syndrome. Am ] Oplitlwlmol 62:8.56-8.59, 1966 4. Katzen LE , Fleischman ]A, Trokel S: YAG laser treatment of cystoid macular edema. Am ] Ophthalmol 9.5:.589-.592 , 1983 .5. Katzen LE, Lapinsky PT, Fleischman JA, Trokel S: YAG laser treatment of cystoid macular edema- clinical update. Cataract 1(2):27-29, 1984 6. Steinert RF, Puliafito CA: The Nd- l:AG Laser in Ophthalmology; Principles and Clillical Applications of Photodisruption. Philadelphia, WB Saunders, 198.5, pp 11.5-123

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7. Gass JDM , Norton EWD: Follow-up study of cystoid macular edema fc)llowing cataract extraction . Trans Am Acad Ophtlwlmol OtollirYllgol 73:665-682 , 1969 8 . Jacobson DR , Dellaporta A: Natural history of cystoid macular edema after cataract extraction. Am] Ophtlwlmol77:445-447 , 1974 9. Kremer M, Baikoff G, Charbonnel B: The release of prostaglandins in human aqueous humour following intraocular surgery. Effect of indomethacin . Prostaglandins 23:695-702 , 1982 10. Martin NF, Green WR, Martin LW: Retinal phlebitis in the Irvine-Gass syndrome. Am] Ophtlwlmol 83:377-386, 1977 11. Michels RG , Green WR , Maumenee AE: Cystoid macular edema following cataract extraction (the Irvine-Gass syndrome). A case studied clinically and histopathologicall y. Ophthalmic Surg 2:217-221. 1971 12. Norton AL, Brown WJ, Carlson M, Pilger IS, et al: Pathogenesis of aphakic macular edema. Am ] Ophthalmol 80:96101 , 1975

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13. Irvine AR. Bresky R, Crowder Bl\I. Forster RK , e tal: Macular ede ma after cataract extraction. A liI! Ophtl/{/lllloI 3:1234- 1240 , 1971 14 . Jaffe NS: Vitreous traction at the posterior pole of the fundus due to alterations in th e vitreous posterior. TIYIII S Am Acad Ophthalmol Otola rYllgol 71:642-651. 1967 15. Fung \VE: The national. prospective, randomized vitrectomv study for chronic aphakic cystoid macular edema. Progress report and comparison b etween the control and nonrandomized groups. Sun Ophtlwlmol 28(Suppl):569-575, 1984 16. Fung WE , Vitrectom y-ACME Study Group: Vitrectomy for chronic aphakic cystoid macular edema: Results of a national , collaborative, prospective , randomized investigation . Ophthalmology 92: 1102-1111 , 1985 17 . Bonnet M, Bievelez B: Iris flu orescein angiographv and I rvineGass' syndrome. Albrecht VOIl Grllefes Arch Klill Exp Ophtlwlmol 213: 187 -194 , 1980 18. The Miami Study Group: Cystoid macular edema in aphakic and pseudophakic eyes . Am ] Oplztha[1Ilo[ 88:45-48, 1979

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