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Photocoagulation to Prevent Retinal Detachment in Acute Retinal Necrosis
Photocoagulation to Prevent Retinal Detachment in Acute Retinal Necrosis PAUL STERNBERG, Jr., MD,t DENNIS P. HAN, MD,2 JULIA H. YEO, MD,3 CHARLES C. BARR, MD,4 HILEL LEWIS, MD/ GEORGE A. WILLIAMS, MD,2 WILLIAM F. MIELER, MD2
Abstract: Retinal detachment (RD) occurs in more than 50% of eyes with acute retinal necrosis (ARN) and is the leading cause of visual loss in this syndrome. In order to decrease the incidence of RD in ARN, the authors treated 12 eyes of 10 patients with prophylactic laser photocoagulation. Retinal detachment occurred in two eyes (17%). Over the same time period, seven eyes with ARN did not receive prophylactic laser treatment, most often because of dense vitreous debris, with a 67% rate of RD. Prophylactic photocoagulation treatment should be considered in the management of patients with ARN. [Key words: acute retinal necrosis syndrome, photocoagulation, retinal detachment, retinitis.] Ophthalmology 95: 1389-1393, 1988
Acute retinal necrosis (ARN) is a rare but devastating syndrome of iritis, vitritis, and vasoocclusive retinitis. I-II In the past few years, immunologic and histologic data have implicated viruses of the herpes family as the causative agent in this disease. 12-16 Because of this, treatment with acyclovir [9-2 (2-hydroxyethoxy methyl) guanine] sodium has been advocated. 17 Such treatment usually results in clinical regression of the active areas of retinitis. However, the visual prognosis remains poor because of retinal detachment (RD), optic nerve damage, and macular damage. Retinal detachment has been reported
Originally received: November 10, 1987. Revision accepted: June 6, 1988. Department of Ophthalmology, Emory University School of Medicine, Atlanta. 2 The Eye Institute, Medical College of Wisconsin, Milwaukee. 3 Wilmer Ophthalmological Institute, Johns Hopkins Medical Institutions, Baltimore. • Department of Ophthalmology, University of Louisville, Louisville.
to occur in 50 to 75% of eyes with ARN.IS Detachments occur from the combination of vitreous traction and retinal tears occurring at the edge of normal and necrotic retina. When they occur, repair can be quite difficult, often resulting in poor visual outcome. In their article describing RD after ARN, Clarkson et al lS raised the issue of prophylaxis against RD, suggesting photocoagulation treatment posterior to the zone of involved retina. Since that time, two reports have described beneficial results from prophylactic photocoagulation in patients with ARN. 19,20 In this article, we report the results in 12 eyes of 10 patients who received prophylactic photocoagulation to prevent RD in the ARN syndrome. In addition, we report the clinical course of six patients seen at our institutions with ARN who did not receive prophylactic treatment.
1
Supported in part by a departmental grant from Research to Prevent Blindness, Inc. Presented at the American Academy of Ophthalmology Annual Meeting, Dallas, November 1987. Reprint requests to Paul Sternberg, Jr., MD, Emory University School of Medicine, Department of Ophthalmology, 1327 Clifton Rd, N.E., Atlanta, GA 30322.
MATERIALS AND METHODS The medical records of patients carrying the diagnosis of ARN at the Emory Eye Center, Medical College of Wisconsin, Wilmer Eye Institute, and University of Louisville were reviewed. Sixteen patients (19 eyes) were seen between August 1984 and March 1987. In all cases, the diagnosis of ARN was established on the basis of the characteristic confluent peripheral vasoocclusive necrotizing retinitis accompanied by varying degrees of anterior 1389
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Fig 1. Prophylactic photocoagulation was applied in two to three rows to create a broad band posterior to the peripheral retinal necrosis.
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VOLUME 95
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NUMBER 10
Photocoagulation was applied as far anteriorly as possible toward the margin of the involved retina. Additional laser treatment was applied when the retinitis progressed through the area of treatment. In two eyes, zones of retinitis involved the posterior retina in addition to the peripheral areas of retinal necrosis. These patients received scatter photocoagulation in addition to treatment of the peripheral areas of necrosis with a confluent band ofphotocoagulation bums at their posterior margin. In six eyes, photocoagulation was performed immediately after initial presentation. In the remaining six eyes, photocoagulation was performed after completion of acyclovir and prednisone treatment which resulted in clearing of the opaque media. In one case, scatter photocoagulation was performed to non necrotic but ischemic retina to stimulate regression of disc neovascularization. In one eye, cryotherapy supplemented photocoagulation at the anterior edge of the necrotic lesions. All patients received medical treatment in conjunction with laser therapy. In most cases, acyclovir was initially administered intravenously and subsequently orally. Eight of the ten patients (10 of 12 eyes) were also treated with systemic corticosteroids.
CASE REPORTS
Fig 2. Case 3. A 31-year-old woman with unilateral ARN. Photocoagulation burns outline areas of regressed retinitis characterized by prominent pigment migration.
segment and vitreous inflammation. During that time, laser photocoagulation was performed in 12 of the 19 eyes. Eight of these eyes have been reported previously (cases 1,2,4,7,8,9 [left eye], 11, and 14). In those patients not receiving photocoagulation, the record was reviewed to determine whether photocoagulation was precluded by dense vitreous debris, patient refusal, minimal retinal involvement, or other reasons. Photocoagulation was applied in a broad band posterior to the area of peripheral retinal necrosis, in two to three rows using a 200- to 500-~m spot size (Fig 1). Power and duration varied in order to achieve a white retinal bum. 1390
Case 3. A 31-year-old black woman presented with a 4-week history of decreased vision in her left eye. She had been treated with topical cycloplegics and corticosteroids, periocular corticosteroids, and systemic corticosteroids before presentation. Her past medical history was unremarkable. Results of examination showed a visual acuity of 20/20 in the right eye and 20/200 in the left. A left afferent pupillary defect was present. Results of slit-lamp examination of the left eye disclosed keratic precipitates, moderate aqueous cell and flare, and prominent vitreous cells and debris. Results of fundus examination showed marked optic nerve swelling. There was prominent venous sheathing and tortuosity. Confluent areas of peripheral retinal whitening with overlying hemorrhage were present from approximately 2 o'clock circumferentially to 10 o'clock. Acyclovir therapy was instituted immediately for 1 week, followed by oral therapy for 2 additional weeks. High-dose oral corticosteroids were continued and were tapered over 1 month. Vitreous debris precluded adequate visualization of the peripheral retinal whitening for prophylactic photocoagulation treatment. However, after 3 weeks of treatment, vitreous debris had cleared, visual acuity had improved to 20/60, and the peripheral areas of retinal whitening had regressed and were replaced by mottled pigment migration. Photocoagulation was applied using two rows of argon photocoagulation at the posterior aspect of the involved retina. Seven hundred eighty-one spots were applied using 500-~m spot size, 0.2 second duration, and a power of approximately 0.5 W. Ten months after presentation, her visual acuity was 20/60. The retina remained attached with a band of photocoagulation bums posterior to the pigment areas of previous retinal necrosis (Fig 2). Case 10. A 71-year-old white man presented with a 2-week history of blurred vision in the right eye. The patient had been noted to have a left pleural effusion 2 months previously. Results of extensive workup including pleural tap, bronchoscopy, and thoracoscopy were all negative. Because of an elevated pleural fluid lymphocyte count, the patient was started on isoniazid,
STERNBERG et al
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PHOTOCOAGULATION IN ARN
despite a negative tuberculosis skin test. However, when blurred vision developed with iritis and retinitis, he was begun on rifampin in addition to the isoniazid. In addition, the patient gave a history of herpes zoster dermatitis which appeared on his right leg 2 months before presentation. On examination, his visual acuity was 20/40 in the right eye and 20/20 in the left. There was no afferent pupillary defect. Results of slit-lamp examination disclosed marked keratic precipitates and moderate aqueous cell and flare. Pigment was present on the anterior lens capsule and there were moderate vitreous cells and debris. Tension was 33 mmHg in the right and 15 mmHg in the left. Results of dilated funduscopic examination showed moderate areas of peripapillary intraretinal whitening with minimal disc swelling. In addition, there were confluent areas of saw-toothed shaped retinal whitening with superficial hemorrhage from approximately 10 to 3 o'clock. The patient was hospitalized and begun on intravenous acyclovir for I week. In addition, he was treated with topical cycloplegics, corticosteroids, and timoptic. Isoniazid and rifampin were continued. After one week, prednisone was added at a dosage of60 mg orally daily. The patient received photocoagulation for 360 0 in a broad band posterior to the area of peripheral retinal whitening. Three rows of photocoagulation burns were placed, with the patient receiving 1122 spots of argon blue green laser of 0.2 second duration, 500-lLm spot size, 0.6 W. Over the next 3 weeks, the patient's vitreous debris increased, and visual acuity dropped to counting fingers. However, the areas of necrotizing retinitis had not progressed past the laser-induced chorioretinal adhesion. Four weeks after photocoagulation, the patient was noted to have an RD from approximately 9 o c' lock clockwise to 6 o'clock with a retinal break developing at the posterior edge of previously necrotic retina at approximately I o'clock anterior to the photocoagulation. The macula was de-
Fig 3. Case 10. A 71-year-old man with ARN underwent successful vitrectomy and scleral buckle for combined traction/rhegmatogenous RD. Prophylactic photocoagulation burns (arrows) are visible superior to the superior temporal arcade beneath the residual epiretinal membrane.
tached. The patient underwent pars plana vitrectomy, scleral buckle, fluid-gas exchange, and supplemental endophotocoagulation. Postoperatively, the retina has remained attached (Fig 3). Visual acuity is 20/60 5 months after surgery.
RESULTS Retinal detachment developed in 2 of 12 eyes treated with laser photocoagulation (17%) (Table 1). In one of
Table 1. Eyes with Acute Retinal Necrosis Receiving Prophylactic Photocoagulation Case No.
Age (yrs)
Eye
120 220 3 419 5
22 29 31 33 33
aD aD as as as
6
38
as
40 63 65
aD aD aD as
71
aD aD
720 820 920
10
VA = visual acuity;
VA at Follow-up
Length of Followup (mos)
Attached Attached Attached Attached Attached after vitrectomy /silicone oil for retinal detachment
20/20 20/100 20/60 20/25 20/300
6 34 10 27 13
Acyclovir/prednisone
Attached with cystoid macular edema
20/200
23
20/25
Acyclovir/prednisone
20/70
23
20/60 20/300 20/25
Acyclovir/prednisone Acyclovir/prednisone Acyclovir /prednisone/ gancyclovir
Attached with cystoid macular edema Attached Attached with peripheral holes Attached with macular hole
20/30 20/40 20/80
23 36 13
20/20 20/40
Gancyclovir Acyclovir / prednisone
Attached Attached after vitrectomy /scleral buckle for retinal detachment
20/20 20/60
4 6
Extent of Fundus Involvement
VA at Presentation
Medical Therapy
Retinal Status at Last Follow-up
4 clock hours 5 clock hours 8 clock hours 6 clock hours 4 clock hours with posterior extension through macula 3 clock hours with isolated areas along arcades Isolated areas along arcades 5 clock hours 5 clock hours 9 clock hours with isolated areas elsewhere 2 clock hours 5 clock hours
20/70 20/400 20/200 20/25 20/60
Acyclovir /prednisone Acyclovir/prednisone Acyclovir/prednisone Acyclovir/prednisone Acyclovir
20/25
aD = right eye; as = left eye. 1391
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Table 2. Eyes with Acute Retinal Necrosis Not Receiving Photocoagulation Case No.
Age (yrs)
Eye
11 19 12
59 62 62
00 OS 00
13 1420 15 16
67 72 80 84
00 00 OS 00
VA
Extent of Fundus Involvement 7 clock hours 12 clock hours Scattered focal areas 8 clock hours 6 clock hours 10 clock hours 7 clock hours with retinal detachment
VA at Presentation
Medical Therapy
3/400 20/400 20/20
Acyclovir/prednisone Acyclovir/prednisone Acyclovir/prednisone
Detached Detached Attached
LP NLP 20/20
HM 20/70 CF LP
Acyclovir/prednisone Acyclovir/prednisone Acyclovir/prednisone Refused therapy
Attached Detached Detached No follow-up
HM HM NLP
VA at Follow-up
= visual acuity; 00 = right eye; LP = light peception; OS = left eye; NLP = no light perception; HM = hand motions; CF = counting fingers.
Table 3. Retinal Detachment Rate in Acute Retinal Necrosis Patients
Laser treatment No laser treatment
Total No. of Eyes
No. of Eyes with Retinal Detachment (%)
12 6
4 (67)
2 (17)
these cases, a large ragged retinal break within a quadrant of retinitis was noted at the time of presentation before placement of photocoagulation. Follow-up ranged from 4 to 36 months (mean, 18 months). During this time period, six patients (7 eyes) with ARN, who were not treated with laser treatment (Table 2), were seen at four institutions. Media were too opaque to permit photocoagulation in five eyes, a preexisting RD precluded photocoagulation in one eye, and in one eye laser treatment was not performed because of minimal retinal disease. Retinal detachments developed in four of the six eyes (67%) without preexisting detachment (Table 3). The RDs in the two patients who received prophylactic photocoagulation were successfully repaired. In one patient, a combination of vitrectomy and scleral buckle reattached the retina with resulting visual acuity of 20/ 60. The other patient required vitrectomy, scleral buckle, and silicone oil injection with final visual acuity of 20/ 300. Of the patients with RDs without prophylactic photocoagulation, three were successfully repaired with vitrectomy and scleral buckling. In all cases, visual acuity was worse than 5/200. In one patient, the retina could not be successfully reattached surgically. Another patient received vitrectomy and endophotocoagulation but the eye became phthisical.
DISCUSSION Although the ARN syndrome was first described in 1971, it is only in the past few years that the high incidence of RD has become apparent. In the retrospective review
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Retinal Status at Last Follow-up
of the literature by Clarkson et al l8 in 1984, RD was identified in 72% of the 63 eyes. Initial attempts to repair these RDs met with poor results, with a cumulative success rate of 22%. However, with the use of vitrectomy techniques combined with scleral buckling, Clarkson et al l8 have achieved 70% reattachment rates. Unfortunately, visual results have been more disappointing with only 4 of 13 eyes obtaining 20/200 or better. Despite successful su~~o/, vision was reduced from optic atrophy related to papillitIs, macular pucker related to the RD, macular involvement from the detachment, or macular retinitis. Retinal detachment usually develops as a result of retinal breaks located at the junction of involved and uninvolved retina. These breaks are often located posteriorly and may be quite large, from an "unzippering" effect. Less frequently, atrophic breaks in necrotic retina can develop in these patients. Vitreous traction, possibly resulting from the accompanying vitritis in the acute phase, may create complex combined traction rhegmatogenous RD. Because of the frequency of RD, the poor visual prognosis and the difficulty of surgical repair, Clarkson et al l8 raised the question of prophylactic photocoagulation in ARN patients. It was hoped that the risk of RD could be diminished by forming a chorioretinal adhesion posterior to the area of necrotic retina. In two previous articles, six eyes received prophylactic photocoagulation with no cases of RD after 6 months of follow_Up.19,20 In this report, there are additional cases, presenting 12 eyes treated with prophylactic laser treatment. We report two eyes developing detachments despite prophylactic laser treatment. At the same time, we have identified seven eyes with ARN, seen at the same institutions over the same time period, in which photocoagulation was not performed whose rate of detachment is consistent with that reported in the literature. The rate of RD was 17% in the eyes treated with photocoagulation versus 67% in the other eyes. Interestingly, when RDs occurred, there was a higher rate of surgical success as well as better visual function in those eyes successfully repaired. The apparent better outcome in the eyes treated with prophylactic photocoagulation may be the result either of
STERNBERG et al
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PHOTOCOAGULATION IN ARN
the laser treatment or a result of these eyes having less severe disease. It is well documented that photocoagulation creates a stronger chorioretinal adhesion than that present before laser treatment. 21 A posterior vitreous detachment that could cause vitreoretinal traction in an area of vitreoretinal adhesion, such as at the edge of involved necrotic retina, is likely to develop in eyes with intraocular inflammation. The stronger chorioretinal adhesion formed by photocoagulation bums could counteract the vitreoretinal traction and prevent RD. On the other hand, tractional as well as combined traction/rhegmatogenous detachments often develop in diabetic patients even in the presence of adequate photocoagulation. In addition, photocoagulation causes retinal damage and can be responsible for atrophic retinal hole formation by itself. No cases of atrophic retinal hole formation developed in any of our lasered eyes in areas receiving photocoagulation. Unquestionably, photocoagulation was used here in cases with less vitreous opacification. If vitreous opacification is an accurate measurement of the severity of the disease process, then prophylactic photocoagulation was used in the less severely involved eyes in this series. When we look at the extent offundus involvement, five of seven eyes not lasered had greater than 6 clock hours of retinitis as opposed to 2 of 12 eyes treated with prophylactic photocoagulation. The fact that so few of the lasered eyes had extensive retinal involvement may indicate that this group of patients had milder ARN. It is interesting that even when RD developed, visual outcome was better in the eyes that had received prophylactic photocoagulation. This may be another indication that the eyes receiving laser treatment had less severe disease. It also, however, may indicate that the prophylactic photocoagulation limited the size of the retinal break and the extent of the RD thereby making surgical repair easier. It is only with a randomized controlled study of laser treatment in ARN that this question can be adequately answered. The rarity ofthe syndrome precludes such a study. Because of the uniformly poor outcome in the eyes that did not receive prophylactic laser treatment, these results suggest that prophylactic photocoagulation treatment should be considered in the management of patients with ARN. Because vitreous opacification often progresses even with regression of acute retinitis areas after antiviral and anti-inflammatory treatment, photocoagulation should be performed as early as possible. In some cases, vitreous opacification may improve with medical treatment. If possible, photocoagulation should then be performed. However, when persistent vitreous debris precludes photocoagulation, these eyes carry a very high likelihood of RDs developing and should be followed closely.
REFERENCES 1. Urayama A, Yamada N, Sasaki T, et al. Unilateral acute uveitis with periarteritis and detachment. Jpn J Clin Ophthalmol 1971; 25:60719. 2. Willerson D Jr. Aaberg TM, Reeser FH. Necrotizing vaso-occlusive retinitis. Am J Ophthalmol1977; 84:209-19. 3. Young NJA, Bird AC. Bilateral acute retinal necrosis. Br J Ophthalmol 1978; 62:581-90. 4. Price FW Jr, Schlaegel TF Jr. Bilateral acute retinal necrosis. Am J Ophthalmol 1980; 89:419-24. 5. Kometani J, Asayama T. A case of specific uveitis occurring acutely in the right eye. Folia Ophthalmol Jpn 1978; 29:1397-401. 6. Bando K, Kinoshita A. Mimura Y. Six cases of so-called 'Kirisawa type' uveitis. Jpn J Clin Ophthalmol1979; 33:1515-21. 7. Okinami S, Tsukahara I. Acute severe uveitis with retinal vasculitis and retinal detachment. Ophthalmologica 1979; 179:276-85. 8. Fisher JP, Lewis ML, Blumenkranz M, et al. The acute retinal necrosis syndrome. Part I: Clinical manifestations. Ophthalmology 1982; 89: 1309-16. 9. Culbertson WW, Blumenkranz MS, Pepose JS, et al. Varicella zoster virus is a cause of the acute retinal necrosis syndrome. Ophthalmology 1986; 93:559-69. 10. Culbertson WW, Blumenkranz MS, Haines H, et al. The acute retinal necrosis syndrome. Part II: Histopathology and etiology. Ophthalmology 1982; 89:1317-25. 11. Sternberg P Jr, Knox DL, Finkelstein D, et aI. Acute retinal necrosis syndrome. Retina 1982; 2:145-51. 12. Rungger-Brandle E, Roux L, Leuenberger PM. Bilateral acute retinal necrosis (BARN): identification of the presumed infectious agent. Ophthalmology 1984; 91 :1648-58. 13. Matsuo T, Date S, Tsuji T, et al. Immune complex containing herpesvirus antigen in a patient with acute retinal necrosis. Am J Ophthalmol 1986; 101 :368-71. 14. Reese L, Sheu MM, Lee F, et al. Intraocular antibody production suggests herpes zoster is only one cause of acute retinal necrosis (ARN). ARVO Abstracts. Invest Ophthalmol Vis Sci 1986; 27(Suppl):12. 15. Freeman WR, Thomas EL, Rao NA, et al. Demonstration of herpes group virus in acute retinal necrosis syndrome. Am J Ophthalmol 1986; 102:701-09. 16. Willig JL, Kaplan HJ, Holland GN, et al. Herpes zoster virus may be only one cause of ARN. Ophthalmology 1986; 93(Final Program Suppl): 83. 17. Blumenkranz MS, Culbertson WW, Clarkson JG, Dix R. Treatment of the acute retinal necrosis syndrome with intravenous acyclovir. Ophthalmology 1986; 93:296-300. 18. Clarkson JG, Blumenkranz M, Culbertson WW, et al. Retinal detachment following the acute retinal necrosis syndrome. Ophthalmology 1984; 91 :1665-8. 19. Yeo JH, Pepose JS, Stewart JA, et al. Acute retinal necrosis syndrome following herpes zoster dermatitis. Ophthalmology 1986; 93: 141822. 20. Han DP, Lewis H, Williams GA, et al. Laser photocoagulation in the acute retinal necrosis syndrome. Arch Ophthalmol 1987; 105: 1051-4. 21. Kain HL. Chorioretinal adhesion after argon laser photocoagulation. Arch Ophthalmol1984; 102:612-5.
1393
Abstract: Retinal detachment (RD) occurs in more than 50% of eyes with acute retinal necrosis (ARN) and is the leading cause of visual loss in this syndrome. In order to decrease the incidence of RD in ARN, the authors treated 12 eyes of 10 patients with prophylactic laser photocoagulation. Retinal detachment occurred in two eyes (17%). Over the same time period, seven eyes with ARN did not receive prophylactic laser treatment, most often because of dense vitreous debris, with a 67% rate of RD. Prophylactic photocoagulation treatment should be considered in the management of patients with ARN. [Key words: acute retinal necrosis syndrome, photocoagulation, retinal detachment, retinitis.] Ophthalmology 95: 1389-1393, 1988
Acute retinal necrosis (ARN) is a rare but devastating syndrome of iritis, vitritis, and vasoocclusive retinitis. I-II In the past few years, immunologic and histologic data have implicated viruses of the herpes family as the causative agent in this disease. 12-16 Because of this, treatment with acyclovir [9-2 (2-hydroxyethoxy methyl) guanine] sodium has been advocated. 17 Such treatment usually results in clinical regression of the active areas of retinitis. However, the visual prognosis remains poor because of retinal detachment (RD), optic nerve damage, and macular damage. Retinal detachment has been reported
Originally received: November 10, 1987. Revision accepted: June 6, 1988. Department of Ophthalmology, Emory University School of Medicine, Atlanta. 2 The Eye Institute, Medical College of Wisconsin, Milwaukee. 3 Wilmer Ophthalmological Institute, Johns Hopkins Medical Institutions, Baltimore. • Department of Ophthalmology, University of Louisville, Louisville.
to occur in 50 to 75% of eyes with ARN.IS Detachments occur from the combination of vitreous traction and retinal tears occurring at the edge of normal and necrotic retina. When they occur, repair can be quite difficult, often resulting in poor visual outcome. In their article describing RD after ARN, Clarkson et al lS raised the issue of prophylaxis against RD, suggesting photocoagulation treatment posterior to the zone of involved retina. Since that time, two reports have described beneficial results from prophylactic photocoagulation in patients with ARN. 19,20 In this article, we report the results in 12 eyes of 10 patients who received prophylactic photocoagulation to prevent RD in the ARN syndrome. In addition, we report the clinical course of six patients seen at our institutions with ARN who did not receive prophylactic treatment.
1
Supported in part by a departmental grant from Research to Prevent Blindness, Inc. Presented at the American Academy of Ophthalmology Annual Meeting, Dallas, November 1987. Reprint requests to Paul Sternberg, Jr., MD, Emory University School of Medicine, Department of Ophthalmology, 1327 Clifton Rd, N.E., Atlanta, GA 30322.
MATERIALS AND METHODS The medical records of patients carrying the diagnosis of ARN at the Emory Eye Center, Medical College of Wisconsin, Wilmer Eye Institute, and University of Louisville were reviewed. Sixteen patients (19 eyes) were seen between August 1984 and March 1987. In all cases, the diagnosis of ARN was established on the basis of the characteristic confluent peripheral vasoocclusive necrotizing retinitis accompanied by varying degrees of anterior 1389
OPHTHALMOLOGY
•
OCTOBER 1988
Fig 1. Prophylactic photocoagulation was applied in two to three rows to create a broad band posterior to the peripheral retinal necrosis.
•
VOLUME 95
•
NUMBER 10
Photocoagulation was applied as far anteriorly as possible toward the margin of the involved retina. Additional laser treatment was applied when the retinitis progressed through the area of treatment. In two eyes, zones of retinitis involved the posterior retina in addition to the peripheral areas of retinal necrosis. These patients received scatter photocoagulation in addition to treatment of the peripheral areas of necrosis with a confluent band ofphotocoagulation bums at their posterior margin. In six eyes, photocoagulation was performed immediately after initial presentation. In the remaining six eyes, photocoagulation was performed after completion of acyclovir and prednisone treatment which resulted in clearing of the opaque media. In one case, scatter photocoagulation was performed to non necrotic but ischemic retina to stimulate regression of disc neovascularization. In one eye, cryotherapy supplemented photocoagulation at the anterior edge of the necrotic lesions. All patients received medical treatment in conjunction with laser therapy. In most cases, acyclovir was initially administered intravenously and subsequently orally. Eight of the ten patients (10 of 12 eyes) were also treated with systemic corticosteroids.
CASE REPORTS
Fig 2. Case 3. A 31-year-old woman with unilateral ARN. Photocoagulation burns outline areas of regressed retinitis characterized by prominent pigment migration.
segment and vitreous inflammation. During that time, laser photocoagulation was performed in 12 of the 19 eyes. Eight of these eyes have been reported previously (cases 1,2,4,7,8,9 [left eye], 11, and 14). In those patients not receiving photocoagulation, the record was reviewed to determine whether photocoagulation was precluded by dense vitreous debris, patient refusal, minimal retinal involvement, or other reasons. Photocoagulation was applied in a broad band posterior to the area of peripheral retinal necrosis, in two to three rows using a 200- to 500-~m spot size (Fig 1). Power and duration varied in order to achieve a white retinal bum. 1390
Case 3. A 31-year-old black woman presented with a 4-week history of decreased vision in her left eye. She had been treated with topical cycloplegics and corticosteroids, periocular corticosteroids, and systemic corticosteroids before presentation. Her past medical history was unremarkable. Results of examination showed a visual acuity of 20/20 in the right eye and 20/200 in the left. A left afferent pupillary defect was present. Results of slit-lamp examination of the left eye disclosed keratic precipitates, moderate aqueous cell and flare, and prominent vitreous cells and debris. Results of fundus examination showed marked optic nerve swelling. There was prominent venous sheathing and tortuosity. Confluent areas of peripheral retinal whitening with overlying hemorrhage were present from approximately 2 o'clock circumferentially to 10 o'clock. Acyclovir therapy was instituted immediately for 1 week, followed by oral therapy for 2 additional weeks. High-dose oral corticosteroids were continued and were tapered over 1 month. Vitreous debris precluded adequate visualization of the peripheral retinal whitening for prophylactic photocoagulation treatment. However, after 3 weeks of treatment, vitreous debris had cleared, visual acuity had improved to 20/60, and the peripheral areas of retinal whitening had regressed and were replaced by mottled pigment migration. Photocoagulation was applied using two rows of argon photocoagulation at the posterior aspect of the involved retina. Seven hundred eighty-one spots were applied using 500-~m spot size, 0.2 second duration, and a power of approximately 0.5 W. Ten months after presentation, her visual acuity was 20/60. The retina remained attached with a band of photocoagulation bums posterior to the pigment areas of previous retinal necrosis (Fig 2). Case 10. A 71-year-old white man presented with a 2-week history of blurred vision in the right eye. The patient had been noted to have a left pleural effusion 2 months previously. Results of extensive workup including pleural tap, bronchoscopy, and thoracoscopy were all negative. Because of an elevated pleural fluid lymphocyte count, the patient was started on isoniazid,
STERNBERG et al
•
PHOTOCOAGULATION IN ARN
despite a negative tuberculosis skin test. However, when blurred vision developed with iritis and retinitis, he was begun on rifampin in addition to the isoniazid. In addition, the patient gave a history of herpes zoster dermatitis which appeared on his right leg 2 months before presentation. On examination, his visual acuity was 20/40 in the right eye and 20/20 in the left. There was no afferent pupillary defect. Results of slit-lamp examination disclosed marked keratic precipitates and moderate aqueous cell and flare. Pigment was present on the anterior lens capsule and there were moderate vitreous cells and debris. Tension was 33 mmHg in the right and 15 mmHg in the left. Results of dilated funduscopic examination showed moderate areas of peripapillary intraretinal whitening with minimal disc swelling. In addition, there were confluent areas of saw-toothed shaped retinal whitening with superficial hemorrhage from approximately 10 to 3 o'clock. The patient was hospitalized and begun on intravenous acyclovir for I week. In addition, he was treated with topical cycloplegics, corticosteroids, and timoptic. Isoniazid and rifampin were continued. After one week, prednisone was added at a dosage of60 mg orally daily. The patient received photocoagulation for 360 0 in a broad band posterior to the area of peripheral retinal whitening. Three rows of photocoagulation burns were placed, with the patient receiving 1122 spots of argon blue green laser of 0.2 second duration, 500-lLm spot size, 0.6 W. Over the next 3 weeks, the patient's vitreous debris increased, and visual acuity dropped to counting fingers. However, the areas of necrotizing retinitis had not progressed past the laser-induced chorioretinal adhesion. Four weeks after photocoagulation, the patient was noted to have an RD from approximately 9 o c' lock clockwise to 6 o'clock with a retinal break developing at the posterior edge of previously necrotic retina at approximately I o'clock anterior to the photocoagulation. The macula was de-
Fig 3. Case 10. A 71-year-old man with ARN underwent successful vitrectomy and scleral buckle for combined traction/rhegmatogenous RD. Prophylactic photocoagulation burns (arrows) are visible superior to the superior temporal arcade beneath the residual epiretinal membrane.
tached. The patient underwent pars plana vitrectomy, scleral buckle, fluid-gas exchange, and supplemental endophotocoagulation. Postoperatively, the retina has remained attached (Fig 3). Visual acuity is 20/60 5 months after surgery.
RESULTS Retinal detachment developed in 2 of 12 eyes treated with laser photocoagulation (17%) (Table 1). In one of
Table 1. Eyes with Acute Retinal Necrosis Receiving Prophylactic Photocoagulation Case No.
Age (yrs)
Eye
120 220 3 419 5
22 29 31 33 33
aD aD as as as
6
38
as
40 63 65
aD aD aD as
71
aD aD
720 820 920
10
VA = visual acuity;
VA at Follow-up
Length of Followup (mos)
Attached Attached Attached Attached Attached after vitrectomy /silicone oil for retinal detachment
20/20 20/100 20/60 20/25 20/300
6 34 10 27 13
Acyclovir/prednisone
Attached with cystoid macular edema
20/200
23
20/25
Acyclovir/prednisone
20/70
23
20/60 20/300 20/25
Acyclovir/prednisone Acyclovir/prednisone Acyclovir /prednisone/ gancyclovir
Attached with cystoid macular edema Attached Attached with peripheral holes Attached with macular hole
20/30 20/40 20/80
23 36 13
20/20 20/40
Gancyclovir Acyclovir / prednisone
Attached Attached after vitrectomy /scleral buckle for retinal detachment
20/20 20/60
4 6
Extent of Fundus Involvement
VA at Presentation
Medical Therapy
Retinal Status at Last Follow-up
4 clock hours 5 clock hours 8 clock hours 6 clock hours 4 clock hours with posterior extension through macula 3 clock hours with isolated areas along arcades Isolated areas along arcades 5 clock hours 5 clock hours 9 clock hours with isolated areas elsewhere 2 clock hours 5 clock hours
20/70 20/400 20/200 20/25 20/60
Acyclovir /prednisone Acyclovir/prednisone Acyclovir/prednisone Acyclovir/prednisone Acyclovir
20/25
aD = right eye; as = left eye. 1391
OPHTHALMOLOGY
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OCTOBER 1988 •
VOLUME 95
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NUMBER 10
Table 2. Eyes with Acute Retinal Necrosis Not Receiving Photocoagulation Case No.
Age (yrs)
Eye
11 19 12
59 62 62
00 OS 00
13 1420 15 16
67 72 80 84
00 00 OS 00
VA
Extent of Fundus Involvement 7 clock hours 12 clock hours Scattered focal areas 8 clock hours 6 clock hours 10 clock hours 7 clock hours with retinal detachment
VA at Presentation
Medical Therapy
3/400 20/400 20/20
Acyclovir/prednisone Acyclovir/prednisone Acyclovir/prednisone
Detached Detached Attached
LP NLP 20/20
HM 20/70 CF LP
Acyclovir/prednisone Acyclovir/prednisone Acyclovir/prednisone Refused therapy
Attached Detached Detached No follow-up
HM HM NLP
VA at Follow-up
= visual acuity; 00 = right eye; LP = light peception; OS = left eye; NLP = no light perception; HM = hand motions; CF = counting fingers.
Table 3. Retinal Detachment Rate in Acute Retinal Necrosis Patients
Laser treatment No laser treatment
Total No. of Eyes
No. of Eyes with Retinal Detachment (%)
12 6
4 (67)
2 (17)
these cases, a large ragged retinal break within a quadrant of retinitis was noted at the time of presentation before placement of photocoagulation. Follow-up ranged from 4 to 36 months (mean, 18 months). During this time period, six patients (7 eyes) with ARN, who were not treated with laser treatment (Table 2), were seen at four institutions. Media were too opaque to permit photocoagulation in five eyes, a preexisting RD precluded photocoagulation in one eye, and in one eye laser treatment was not performed because of minimal retinal disease. Retinal detachments developed in four of the six eyes (67%) without preexisting detachment (Table 3). The RDs in the two patients who received prophylactic photocoagulation were successfully repaired. In one patient, a combination of vitrectomy and scleral buckle reattached the retina with resulting visual acuity of 20/ 60. The other patient required vitrectomy, scleral buckle, and silicone oil injection with final visual acuity of 20/ 300. Of the patients with RDs without prophylactic photocoagulation, three were successfully repaired with vitrectomy and scleral buckling. In all cases, visual acuity was worse than 5/200. In one patient, the retina could not be successfully reattached surgically. Another patient received vitrectomy and endophotocoagulation but the eye became phthisical.
DISCUSSION Although the ARN syndrome was first described in 1971, it is only in the past few years that the high incidence of RD has become apparent. In the retrospective review
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Retinal Status at Last Follow-up
of the literature by Clarkson et al l8 in 1984, RD was identified in 72% of the 63 eyes. Initial attempts to repair these RDs met with poor results, with a cumulative success rate of 22%. However, with the use of vitrectomy techniques combined with scleral buckling, Clarkson et al l8 have achieved 70% reattachment rates. Unfortunately, visual results have been more disappointing with only 4 of 13 eyes obtaining 20/200 or better. Despite successful su~~o/, vision was reduced from optic atrophy related to papillitIs, macular pucker related to the RD, macular involvement from the detachment, or macular retinitis. Retinal detachment usually develops as a result of retinal breaks located at the junction of involved and uninvolved retina. These breaks are often located posteriorly and may be quite large, from an "unzippering" effect. Less frequently, atrophic breaks in necrotic retina can develop in these patients. Vitreous traction, possibly resulting from the accompanying vitritis in the acute phase, may create complex combined traction rhegmatogenous RD. Because of the frequency of RD, the poor visual prognosis and the difficulty of surgical repair, Clarkson et al l8 raised the question of prophylactic photocoagulation in ARN patients. It was hoped that the risk of RD could be diminished by forming a chorioretinal adhesion posterior to the area of necrotic retina. In two previous articles, six eyes received prophylactic photocoagulation with no cases of RD after 6 months of follow_Up.19,20 In this report, there are additional cases, presenting 12 eyes treated with prophylactic laser treatment. We report two eyes developing detachments despite prophylactic laser treatment. At the same time, we have identified seven eyes with ARN, seen at the same institutions over the same time period, in which photocoagulation was not performed whose rate of detachment is consistent with that reported in the literature. The rate of RD was 17% in the eyes treated with photocoagulation versus 67% in the other eyes. Interestingly, when RDs occurred, there was a higher rate of surgical success as well as better visual function in those eyes successfully repaired. The apparent better outcome in the eyes treated with prophylactic photocoagulation may be the result either of
STERNBERG et al
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PHOTOCOAGULATION IN ARN
the laser treatment or a result of these eyes having less severe disease. It is well documented that photocoagulation creates a stronger chorioretinal adhesion than that present before laser treatment. 21 A posterior vitreous detachment that could cause vitreoretinal traction in an area of vitreoretinal adhesion, such as at the edge of involved necrotic retina, is likely to develop in eyes with intraocular inflammation. The stronger chorioretinal adhesion formed by photocoagulation bums could counteract the vitreoretinal traction and prevent RD. On the other hand, tractional as well as combined traction/rhegmatogenous detachments often develop in diabetic patients even in the presence of adequate photocoagulation. In addition, photocoagulation causes retinal damage and can be responsible for atrophic retinal hole formation by itself. No cases of atrophic retinal hole formation developed in any of our lasered eyes in areas receiving photocoagulation. Unquestionably, photocoagulation was used here in cases with less vitreous opacification. If vitreous opacification is an accurate measurement of the severity of the disease process, then prophylactic photocoagulation was used in the less severely involved eyes in this series. When we look at the extent offundus involvement, five of seven eyes not lasered had greater than 6 clock hours of retinitis as opposed to 2 of 12 eyes treated with prophylactic photocoagulation. The fact that so few of the lasered eyes had extensive retinal involvement may indicate that this group of patients had milder ARN. It is interesting that even when RD developed, visual outcome was better in the eyes that had received prophylactic photocoagulation. This may be another indication that the eyes receiving laser treatment had less severe disease. It also, however, may indicate that the prophylactic photocoagulation limited the size of the retinal break and the extent of the RD thereby making surgical repair easier. It is only with a randomized controlled study of laser treatment in ARN that this question can be adequately answered. The rarity ofthe syndrome precludes such a study. Because of the uniformly poor outcome in the eyes that did not receive prophylactic laser treatment, these results suggest that prophylactic photocoagulation treatment should be considered in the management of patients with ARN. Because vitreous opacification often progresses even with regression of acute retinitis areas after antiviral and anti-inflammatory treatment, photocoagulation should be performed as early as possible. In some cases, vitreous opacification may improve with medical treatment. If possible, photocoagulation should then be performed. However, when persistent vitreous debris precludes photocoagulation, these eyes carry a very high likelihood of RDs developing and should be followed closely.
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