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Al-Shifa Journal of
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Aims and Scope
Ocular Infections and Seasonal Variations Sensitivity of Tests in Dry Eyes Intravitreal Kenacort in Macular Edema ERG in Diagnosis of Retinal Problems |
Role of intravitreal triamcinolone acetonide injection in treating refractory diabetic macular edema Nadeem Ishaq, MBBS, MCPS, FCPS Purpose: To study the effect of intravitreal triamcinolone in patients with diffuse macular edema refractory to laser treatment.
Methodology: Intravitreal injection of triamcinolone acetonide 4 mg in 0.1 ml was given through a 27-g needle in the inferotemporal pars plana 3.5 mm posterior to the limbus under topical anesthesia. After the injection, IOP, indirect ophthalmoscopy, fundus examination was carried out to evaluate the perfusion of the central retinal artery and the intravitreal location of the triamcinolone. Results: Improvement in visual acuity was found in 39[82%] patients. The mean improvement of acuity was 1,2,4,2 Snellen lines at the 6wks, 8wks, 12wks, and 24 wks follow-up intervals respectively. Intraocular pressure increase was observed in 21[44%] eyes. At 12 wks follow-up only 2 eyes had persistence of high IOP up to 32 mm Hg and received combination therapy of topical prostaglandin analog and beta blockers. Two eyes exhibited cataract progression at six months. Re-injection was performed after six months in 13[27%] of 47 because of recurrence of diabetic macular edema. Conclusion: Intravitreal triamcinolone is a promising therapy for patients with diabetic macular edema refractory to laser treatment. It is effective in improving vision, reducing macular thickness and inducing re-absorption of hard exudates. Al-Shifa Journal of Ophthalmology 2005; 1: 30-33 © Al-Shifa Trust Eye Hospital, Rawalpindi, Pakistan. |
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| Diabetic retinopathy is the leading cause of blindness in patients aged more than 50 years in our country. Among them Macular edema is the main reason of reduced vision in this population. According to the ETDRS study, laser photocoagulation reduced the risk of moderate visual acuity loss for all eyes with diabetic macular edema and mild to moderate non-proliferative diabetic retinopathy by about 50 percent.1 However, 12 percent of the treated eyes still lost 15 or more ETDRS letters at the three-year follow-up interval. Furthermore, less than 3 percent of treated eyes demonstrated an improvement in visual acuity of the same magnitude. The exact mechanism of action of corticosteroids in the treatment of macular edema is unknown. Brooks McCuen, MD, and colleagues demonstrated the lack of ocular toxicity of intravitreal triamcinolone acetonide in an experimental rabbit model2. The rationale behind their use lies in their ability to inhibit the arachidonic acid pathway, of which prostaglandin is a product. Corticosteroids may also down regulate the production of vascular endothelial growth factor. In addition, triamcinolone acetonide has been shown to reduce the breakdown of the blood-retinal barrier3. It is accepted that in diabetic macular edema there is a breakdown of the blood-retina barrier, and that prostaglandin and intravitreal anti-vascular endothelial growth/permeability factor (VEGF) may play a role in this process. Adam Martidis, MD, and his coworkers recently reported on the use of IVTA at the dose of 4 mg in 0.1 mL for the treatment of refractory diabetic macular edema4. |
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Originally received: June 10, 2004 |
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Methodology This study was conducted at Retina Unit at Al-Shifa Trust eye hospital. These patients’ presented with diffuse diabetic macular edema, all of which had sustained, steady, poor visual acuity ranging from 6\60 to 6/24 even after modified grid laser treatment. After obtaining informed consent from the patients the intravitreal injection was performed under topical anesthesia. A lid speculum was used to keep the eyelashes away from the conjunctiva. Povidone iodine 5% eye drops and Ciprofloxacin eye drops were instilled in the conjunctiva every minute for three times. The injection of triamcinolone acetonide 4 mg in 0.1 ml was given through a 27-g needle in the inferotemporal pars plana 3.5 mm posterior to the limbus. After the injection, IOP, indirect ophthalmoscopy, fundus examination was carried out to evaluate the perfusion of the central retinal artery and the intravitreal location of the triamcinolone. Results54 eyes of 42 patients were enrolled in this study. 10 patients had bilateral intravitreal Kenacort-A injection but at the different times. 47 eyes of 43 patients had regular follow up. Five Patients with 7[13%] eyes were lost to follow-up. Out of 47, 12[25%] eyes completed 6 month follow up and 31[65%] eyes completed 4 months follow-up and remaining 4[8%] eyes completed 8weeks follow-up. 8[17%] eyes showed no significant improvement in Snellen acuity. Out of these, 2 developed significant cataract and remaining 6 had hard exudates plaque at fovea We found improvement in visual acuity in 39[82%] patients. The mean improvement of acuity was 1,2,4,2 Snellen lines at the 6wks, 8wks, 12wks, and 24 wks follow-up intervals respectively. Intraocular pressure increase was observed in 21[44%] Eyes. The mean rise in IOP was 5±1. At 6 wks follow up 19[89%] eyes showed normal IOP, while at 12 wks follow-up only 2 eyes had persistence of high IOP up to 32 mm Hg and received combination therapy of topical prostaglandin analog and beta blockers. Two eyes exhibited cataract progression at six months. The commonest complaint was diffuse hazy curtain in front of the eyes that gradually decreased over the period of two weeks. No other complications were noted over a mean follow-up of 6.2 months. Re-injection was performed after six months in 13[27%] of 47 because of recurrence of diabetic macular edema.
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Discussion Diffuse macular edema is one of the most intractable complications of diabetic retinopathy5. The development is usually insidious and laser treatment is only very occasionally successful in improving visual acuity. Injection of triamcinolone has been used by a number of other investigators. It is slowly absorbed from the vitreous over a period of several months6, whereas cortisone would be absorbed within a few hours. Intravitreal steroids have been used for inflammatory eye disease7. Recent work suggests that there is probably an inflammatory component in diabetic retinopathy; the white blood cells are involved in the vascular occlusion leading to manifestations of retinopathy. We have been using intravitreal triamcinolone acetonide for the treatment of refractory diabetic macular edema at retina clinic Al-Shifa Trust eye hospital and we have noted resolution of the macular edema and subjective and objective improvement in vision after intravitreal triamcinolone acetonide Studies have shown that intravitreal triamcinolone acetonide is effective in improving Snellen acuity as well as contrast sensitivity. Such a positive effect reaches its maximum 6weeks to 16 weeks after the intravitreal triamcinolone treatment. This is followed by a decline in vision. Repeated intravitreal triamcinolone treatment is effective in determining fresh improvement in visual acuity. Thus over 2 lines’ improvement in visual acuity on the Snellen chart was noted by Martidis et al.4 and, even after 6 months, 1.5 lines’ improvement was recorded. In the present study, vision showed significant improvement, from 2 ± 1-Snellen lines in first 8 weeks and the maximum of 4 ± 1 Snellen lines in first 16 weeks. There is gradual decline of 2± 1 Snellen lines in 6 month follow up. In conclusion, intravitreal triamcinolone is a promising therapy for patients with diabetic macular edema refractory to laser treatment. It is effective in improving vision, reducing macular thickness and inducing re-absorption of hard exudates. Whilst triamcinolone may be a useful addition to the therapeutic armamentarium in macular edema, the role of laser photocoagulation is definitely to reduce the demand of oxygen but there is no definitive treatment to prevent the underlying causes of leakage. Intravitreal anti-vascular endothelial growth/permeability factor (VEGF) is currently being used in clinical trials in age-related macular degeneration7, and may be used in the future for this condition as well. Since protein kinase C inhibitor has been shown to be successful at reducing VEGF-induced leakage in rats, it is possible that it could also be applied in humans8.
References 2. McCuen BW II, Bessler M, Tano Y, et al. The lack of toxicity of intravitreally administered triamcinolone acetonide. Am J Ophthalmol 1981;91:785-788 3. Wilson CA, Berkowitz BA, Sato Y, et al. Treatment with intravitreal steroids reduces blood-retina barrier breakdown due to laser photocoagulation. Arch Ophthalmol 1992;110:155-159. 4. Martidis A, Duker JS, Greenberg PB, et al. Intravitreal triamcinolone for refractory diabetic macular edema. Ophthalmology 2002;109:920-927. 5. Jonas JB, Kreissig I, Sofker A, Degenring RF. Intravitreal injection of triamcinolone for diffuse diabetic macular edema. Arch Ophthalmol 2003;121:57-61. 6. Beer PM, Bakri SJ, Singh RJ, et al. Intraocular concentration and pharmacokinetics of triamcinolone acetonide after a single intravitreal injection. Ophthalmology 2003;110:681-686 7. Martidis A, Duker JS, Greenberg PB, et al. Intravitreal triamcinolone for refractory diabetic macular edema. Ophthalmology 2002;109:920-927. 8. Saraiva VS, Sallum JM, Farah ME. Treatment of cystoid macular edema related to retinitis pigmentosa with intravitreal triamcinolone acetonide. Ophthalmic Surg Lasers Imaging 2003;34:398-400. |
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