The rationale of argon green laser photocoagulation for diabetic maculopathy.
Dept of Ophthalmology, Seth GS Medical College, Parel, Bombay, Maharashtra.
Y K Dastur
Dept of Ophthalmology, Seth GS Medical College, Parel, Bombay, Maharashtra.
Eighty-four patients of bilateral diabetic retinopathy were divided into 2 groups: Group I comprised of 60 patients (mean age 46 yrs) having non-proliferative diabetic retinopathy with maculopathy (total no. of eyes = 120). Group II consisted of 24 patients (mean age 49.1 yrs) with proliferative diabetic retinopathy with maculopathy (total no. of eyes under study = 48). One eye of each patient in group I was treated as a control and the other was subjected to focal laser therapy. While 48/60 control Group I eyes (80%) had 6/24 vision at the outset, at one year follow-up only 39/60 cases (65%) had 6/24 vision. Diabetic maculopathy persisted in all the 60 control eyes at one year. In contrast, 44/60 eyes (73%) subjected to focal laser therapy in Group I, had 6/24 vision at outset but one year later, 49/60 eyes (81%) had 6/24 vision. Maculopathy completely regressed in 48/60 eyes (80%). The 48 eyes of Group II patients were subjected to focal and scatter laser therapy. 20/48 eyes (41.6%) had 6/24 vision prior to treatment but one year after treatment, 25/48 eyes (52%) had 6/24 vision. Neovascularization and macular edema regressed after one year in 42/48 eyes (87.1%) and only 4/48 eyes (8.3%) developed localized vitreous hemorrhage. Laser therapy in Group I improved visual acuity by reducing macular edema. In Group II, it improved the vision and reduced the risk of vitreous hemorrhage, detachment and glaucoma.
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Dastur Y K. The rationale of argon green laser photocoagulation for diabetic maculopathy. J Postgrad Med 1994;40:13-7
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Dastur Y K. The rationale of argon green laser photocoagulation for diabetic maculopathy. J Postgrad Med [serial online] 1994 [cited 2022 May 19 ];40:13-7
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Diabetic maculopathy is one of the leading causes of reduced vision in cases of non-proliferative and proliferative diabetic retinopathy. Non-proliferative diabetic retinopathy with maculopathy is generally treated with focal macular grid technique using Argon-green laser,,,,,. However, in cases of proliferative diabetic retinopathy with maculopathy usually focal technique is combined with scatter therapy,,,,,,.
The present study was conducted with a view to determine whether focal laser therapy results in visual recovery and regression of macular edema in patients with non-proliferative diabetic retinopathy with maculopathy. It was also decided to treat patients with proliferative diabetic retinopathy with combined focal and scatter laser therapy to determine whether there is visual recovery and regression of risk factors like neovascularization and macular edema. A follow-up for one year period after laser therapy was planned to evaluate the occurrence of complications like vitreous haemorrhage, tractional retinal detachment and rubeotic glaucoma in these patients.
Eighty-four patients of bilateral diabetic retinopathy were selected for this prospective study. Cases of unilateral or asymmetrical diabetic retinopathy, those photocoagulated elsewhere, cases which might not follow-up regularly for one year, cases of advanced cataract, aphakia, rubeotic glaucoma, tractional retinal detachment and vitreous haemorrhage were not included for this study.
The best corrected visual acuity was assessed before the start of treatment. All patients underwent examination by slit lamp, tonometry, ophthalmoscopy and fluorescein fundus angiography.
Diabetic maculopathy was diagnosed by ophthalmoscopic evidences of microaneurysms, retinal haemorrhages, exudates, venous looping or beading and intraretinal microvascular anomalies. The proliferative diabetic retinopathy was diagnosed by ophthalmoscopic evidences of neovascularization elsewhere and signs of diabetic maculopathy described above.
The patients were divided into 2 groups: Group I comprised of patients with non-proliferative diabetic retinopathy with maculopathy (n=24). The age of patients in Group I ranged from 32-56 yrs (mean- 46 yrs) and 28 of them had insulin dependent diabetes while the rest (32) had non-insulin dependent diabetes. Male to female ratio was 38:22. The Group II included 8 males and 16 females (age range: 36-58 yr; mean being 49.1 yr). Of these, 9 had non-insulin dependent diabetes [Table:1].
Fluorescein fundus angiography was done in all patients using 5 ml of 10% fluorescein injected intravenously. Seventy-two eyes of 36 patients in Group I had an exudative type of maculopathy with focal leakage and good capillary perfusion and 48 eyes of 24 patients in Group I had edematous type of maculopathy with good capillary perfusion and diffuse areas of leakages.
In Group II, 20 eyes of 10 patients had exudative maculopathy and 28 eyes of 14 patients had edematous maculopathy. Both Group I and II did not have any patient having the ischemic type of maculopathy with large areas of capillary non-perfusion. All patients were examined for systemic hypertension and post- lunch blood sugar.
One eye of patients in group I was observed without photocoagulation for one year and the other eye, generally with similar or lower visual acuity or the more advanced maculopathy, was treated by focal Argon green laser using the focal macular grid technique. About 50 - 200 shots of 100 micron size were placed perifoveally encircling the fovea and reaction spots were placed with a spot size distance apart. Faint white reaction was produced at the edge of foveal a vascular zone using 200 - 300 mW power 0.1 second duration. In areas of diffuse leakages, reaction spots were placed confluently, again avoiding the foveal avascular zone. Reaction spots were also placed at the site of leakages, microaneurysm and exudates.
All patients in Group II were high-risk cases and hence both the eyes of these patients were treated by focal and scatter therapy using Argon green laser employing 1600 -2000 shots placed over two sessions. Five hundred micron spot size was used with 500-700 mW power and 0.10 seconds duration. The reaction spots were placed from disc to equator. Reaction spots were placed a spot size apart.
Patients from both the groups were followed up at 3 weekly intervals after photocoagulation for one year. Fundus examination, fluorescein angiography and visual acuity assessment was done at 6 weeks, 6 months and 1 year after photocoagulation. Four lasered eyes of diabetic maculopathy in Group I, which continued to show leakages on fluorescein angiography were retreated with focal therapy at 6 weeks. Group II eyes that continued to show neovascularization of optic disc or elsewhere and macular edema were retreated at 3 months with combined focal and scatter laser therapy.
Sixty patients of Group 1 included 72 eyes of exudative type of maculopathy and 48 eyes of edematous type of maculopathy. 48/60 control eyes (80%) had 6/ 24 vision at outset but after one year, 39/60 control eyes (65%) had 6124 vision [Table:2].
Nearly 80% of the control eyes, lost one line on Snellen's visual acuity chart after one year. On fundus examination and fluorescein angiography, macular edema persisted in all the 60 control eyes and minimally regressed spontaneously in 4 eyes (6.6%). Ail these eyes with regression of macular edema had the exudative type of maculopathy at the outset. Exudates, haemorrhages and microaneurysms persisted in all 60 control eyes [Table:3].
In contrast, in the eyes subjected to focal laser therapy, Group 1 patients showed the following findings: 44/60 eyes (73%) had 6/24 vision at the outset. One year later, 49/60 eyes (81 %) had 6/24 vision [Table:2]. Nearly 33% of Group I eyes subjected to laser therapy, had visual recovery of one line on Snellen's visual acuity chart after one year. On fundus examination and fluorescein angiography after one year, macular edema was found to regress completely in 48/60 lasered eyes (80%) and partially in 10/60 eyes (16.6%) and was found same in 2/60 eyes (3.4%). These 12 eyes with partial or no regression of macular edema had edematous maculopathy at the outset. Exudates, haemorrhages and microaneurysms disappeared in all 60 eyes after one year of laser therapy [Table:3].
Forty-eight eyes in Group II included 20 with exudative type of maculopathy and 28 with edematous type of maculopathy. 20/48 eyes (41.0%) had 6/24 vision at outset but after laser therapy and 1 year follow-up 25/48 eyes (52%) had 6/24 vision [Table:4].
On fundus examination and fluorescein angiography, it was observed that one year later, in lasered eyes, only 6/48 eyes (12.5%) had neovascularization of optic disc, 8/44 eyes (18.1%) had neovascularization elsewhere and only 3/48 eyes (6.2%) had persistent macular edema [Table:5].
The 3 eyes with persistent macular edema had oedematous type of maculopathy at the outset. During 1 year follow-up, only 4/48 eyes (8.3%) developed a localized vitreous haemorrhage.
Diabetic maculopathy is an important cause of visual loss in eyes with both non-proliferative and proliferative diabetic retinopathy. Eyes with non-proliferative retinopathy with maculopathy were treated in this study by focal macular grid therapy using Argon green laser,,,,,. Argon green was preferred to Argon blue because it has good haemoglobin absorption in retinal blood vessel causes minimal damage to macular xanthophyll and retinal nerve fibre layer. In this study, of 60 control eyes of patients in Group I, 16 had 6/12 vision (27%) in the beginning but after one year of observation, only 3/60 (5%) eyes had 6/12 vision. Persistence of macular edema was unchanged in 56/ 60 eyes (93.4 %) and it partially regressed in 4 eyes (6.6%). Other signs like microaneurysms, haemorrhages and exudates persisted in all these 60 control eyes. The other eye of each of the Group I patients was treated by focal macular grid Argon green laser. At the outset, 12/60 eyes had 6/12 vision and 1 year later 18/60 eyes (30%) had 6/12 vision. Microaneurysms, exudates and haemorrhages were found to disappear in all 60 lasered eyes after 1 year of therapy. Diabetic macular edema completely regressed in 48/60 eyes (80%), partially regressed in 10 eyes (16.6%) and remained unchanged in 2 eyes (3.4%). Focal macular grid Argon green therapy results in the production of paracentral scotomas, which tend to decrease gradually over a period of time 2.6. Blankenship' reported that 58% eyes after focal Argon green laser therapy had 6/12 vision after a 15 year follow - up. In our study with a follow up of only one year 18/60 eyes (30%) had 6/12 vision after focal Argon laser therapy. Gandric et al have stated that extramacular focal Argon laser therapy is less effective in controlling macular edema than the perifoveal macular grid therapy employed in this study. This study shows that 33% of treated eyes had one line improvement in Snellen's visual acuity chart in contrast to nearly 80% of control eyes, which lost one line on Snellen's visual acuity chart at 1 year follow-up. After a similar study OW, had reported that 33% lasered eyes improved after 1 year and 45% improved after 2 years and that nearly 27% of observed eyes had a worsening of visual acuity after 1 year follow up. Olk has also reported a patient developing premacular fibroplasia in one eye, which was treated twice with focal laser therapy. However in our study 4 cases, which were retreated with focal laser therapy, did not show any premacular fibroplasia. Two of these cases had persistent macular edema after 1 year follow up.
Both the eyes of patients with proliferative diabetic retinopathy (Group 11:48 eyes) were treated with focal macular grid therapy, followed at the same session by scatter therapy with Argon green laser. This approach reduces the chances of worsening of macular edema, which is likely to occur if only scatter therapy is employed,. In our study 2/48 eyes (4%) had 6/12 vision prior to laser therapy and after 1 year of laser therapy 3/48 eyes (6%) had 6/12 vision. Regression of neovascularization of optic disc occurred within 6 weeks in 36/48 eyes (75%), regression of neovascularization at other sites in 31/44 eyes (70%) and tegression of macular edema in 34/48 eyes (70%). It has been reported following similar studies,, that regression of neovascularization and macular edema occurred in 72% of proliferative diabetic retinopathy cases within 3 weeks of laser therapy. Further, other workers have advised that persistent neovascularization after laser therapy should be retreated,,,. In our study retreatment with laser was required in 14/48 eyes. Following 1 year of therapy, (12.5%) had optic disc neovasularization. 8/44 eyes (18.1%) had neovasculrization elsewhere and 3/48 eyes (6.2%) had persistent macular edema four eyes (8.3%) developed localised vitreous haemorrhage. Bensen has stated that even after ablation of 92% of the retinal area by laser, 7% of the cases of proliferative diabetic retinopathy have severe visual loss. However in our study with one year follow-up none of the eyes developed rubeotic glaucoma fractional retinal detachment or total vitreous haemorrhage.
The study shows that in patients with non-proliferative diabetic retinopathy focal macular grid therapy by Argon green laser facilitates improvement of visual acuity as it causes a regression of macular edema, while eyes without such treatment continue to have progressive visual loss due to persistent macular edema. In patients with proliferative retinopathy combined focal and scatter Argon green laser therapy improves the visual acuity and facilitates regression of neovascularization and macular edema. Further it reduces the chances of severe visual loss due to vitreous haemorrhage, tractional retinal detachment and rubeotic glaucoma.
Olk RJ. Argon green (514 nm) versus Krypton red (647 nm) modified grid laser photocoagulation for diffuse diabetic macular edema. Ophthalmology 1990; 97:1101-1113.|
|2||Early treatment diabetic retinopathy study research group. Early photocoagulation for diabetic retinopathy: ETDRS report No.g. Ophthalmology 1991; 98:766-785.|
|3||Gandric A, Ramioul E, Chaine G. Coscas G. Treatment of diabetic cystoid macular edema by photocoagulation with Argon laser. J Fr Ophthalmol 1984; 7:291-304|
|4||Early treatment diabetic retinopathy study research group. Photocoagulation for diabetic macular edema. ETDRS report No. 1. Arch Ophthalmol 1985; 103:1796-1806.|
|5||Fredricks FI, Marvin PJ, Mathew DD. Macular edema in diabetic retinopathy study patients: diabetic retinopathy study report, No. 12. Ophthalmology 1987; 94:754-760.|
|6||Olk RJ. (Group II: 48 eyes) Modified grid Argon (blue-green) laser photocoagulation for diffuse diabetic macular edema. Ophthalmology 1986; 93:938-950.|
|7||Blankenship GW. Fifteen year Argon laser and xenon photocoagulation results of Bascom Palmer Eye Institute's patients participating in the Diabetic Retinopathy study. Ophthalmology 1991; 98:125-128.|
|8||Doft BH, Blankenship G. Retinopathy risk factor regression after laser panretinal photocoagulation for proliferative diabetic retinopathy. Ophthalmology 1984; 91:1453-1457.|
|9||Little HL. Treatment of proliferative diabetic retinopathy. Long term results of Argon laser photocoagulation. Ophthalmology 1985; 92:279-283. |
|10||Vine AK. The efficacy of additional Argon laser photocodgulation for persistent severe proliferative diabetic retinopathy. Ophthalmology 1985; 95:1532-1537.|
|11||Blankenship GW. A clinical comparison of central and peripheral Argon laser Panretinal photocoagulation for proliferative diabetic retinopathy. Ophthalmology 1988; 95:170-177.|
|12||Kaufman SC, Ferris FL, Seigel DG, Davis MD, DeMets DL. Factors associated with visual outcome after photocoagulation for diabetic retinopathy: diabetic retinopathy study report. Invest Ophthalmol Vis Sci 1989; 30:23-28.|
|13||Bensen WE. Retina In: Laibson PR, editor. Year Book of Ophthalmology, 1990. Chicago: Year Book Medical Publishers; 1990, pp 207-208.