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  Vol. 120 No. 9, September 2002 TABLE OF CONTENTS
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Intravitreous Triamcinolone Acetonide as Treatment for Macular Edema From Central Retinal Vein Occlusion

Arch Ophthalmol. 2002;120:1217-1219.

Central retinal vein occlusion (CRVO) is a common retinal vascular disorder that can lead to significant visual disability. Persistent macular edema is one of the major complications associated with CRVO. The Central Vein Occlusion Study1 evaluated the efficacy of macular grid laser photocoagulation in patients with macular edema caused by CRVO. This study did not find a difference in visual acuity between treated and untreated eyes at any stage during the follow-up period. Therefore, there is currently no proven management for macular edema in the setting of CRVO. The purpose of this interventional case report is to describe the clinical course of 2 patients with macular edema secondary to CRVO who underwent intravitreous injection of triamcinolone acetonide.

Report of Cases

Case 1

A 57-year-old man had a 2-month history of decreased visual acuity in his right eye. On initial examination, his best-corrected visual acuity was 20/40 OD and 20/20 OS. Results of anterior segment examination were remarkable only for 2+ nuclear sclerosis in both eyes. Intraocular pressure was 15 mm Hg OD and 19 mm Hg OS. A dilated fundus examination revealed findings consistent with nonischemic CRVO in the right eye. Macular edema was present. Fundus examination results were normal in the left eye.

Slitlamp biomicroscopy revealed some improvement in the degree of macular edema in the right eye during the next 2 months. However, 8 months after initial examination, his visual acuity had decreased further. Examination at that time revealed a visual acuity of 20/200 OD and 20/20 OS. A dilated fundus examination of the right eye revealed a nonischemic CRVO with significantly increased macular edema (Figure 1A). Optical coherence tomography (OCT) revealed a diffusely thickened retina as well as cystic foveal changes (Figure 1B). The patient was observed for an additional month, and when there was no improvement in the degree of macular thickening or visual acuity, an intravitreous injection of 4 mg (40 mg in 1.0 mL) of triamcinolone acetonide was given in the right eye.



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Figure 1. A, Color fundus photograph of the right eye shows nonischemic central retinal vein occlusion complicated by macular edema before intravitreous injection of triamcinolone acetonide. Visual acuity was 20/200. B, Optical coherence tomogram of the right eye shows a diffusely thickened retina (to 600 µm) before intravitreous injection of triamcinolone acetonide.


Follow-up 1 month later showed a return of visual acuity to 20/25 OD, with complete resolution of macular edema on both clinical examination (Figure 2A) and OCT (Figure 2B). Intraocular pressure was unchanged, and the improvement in visual acuity and clinical examination results remained at the 6-month follow-up.



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Figure 2. A, Color fundus photograph of the right eye 1 month following intravitreous injection of triamcinolone acetonide shows resolution of macular edema. B, Optical coherence tomogram of the right eye 1 month following intravitreous injection of triamcinolone acetonide shows restoration of normal foveal architecture. The central foveal thickness measured 100 µm.


Case 2

A 67-year-old man had a 1-month history of decreased visual acuity in the left eye. Examination revealed a best-corrected visual acuity of 20/20 OD and 20/200 OS. Anterior segment examination results were remarkable for 2+ nuclear sclerosis in both eyes. His intraocular pressure was 10 mm Hg OU. A dilated fundus examination revealed a normal fundus in the right eye. Examination of the left fundus revealed findings consistent with an ischemic CRVO. Foveal thickness was greater than 600 µm on OCT.

The patient was followed up at 2-month intervals for the next 8 months. Although the intraretinal hemorrhage cleared significantly, there was neither improvement in visual acuity nor a decrease in the amount of macular edema noted on clinical examination or OCT.

Because there was no clinical improvement, an intravitreous injection of 4 mg of triamcinolone acetonide (40 mg in 1.0 mL) was given. Figure 3 shows the extensive macular edema noted on both slitlamp biomicroscopy and OCT 5 days before treatment. Three weeks following treatment, his visual acuity improved to 20/100 OS, and a fundus examination revealed a significant decrease in macular edema. Foveal thickness measured with OCT was 100 µm. At the 2-month follow-up, there continued to be a reduction in macular edema on clinical examination and OCT (Figure 4).



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Figure 3. A, Color fundus photograph of the left eye shows ischemic central retinal vein occlusion complicated by macular edema before intravitreous injection of triamcinolone acetonide. This photograph was taken 8 months after initial examination, and although there was reduction in the amount of intraretinal hemorrhage, significant macular edema persisted. Visual acuity was 20/200. B, Optical coherence tomogram of the left eye shows cystic foveal changes and a diffusely thickened retina (to >600 µm) before intravitreous injection of triamcinolone acetonide.




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Figure 4. A, Color fundus photograph of the left eye 2 months following intravitreous injection of triamcinolone acetonide shows resolution of macular edema. A reduction in the amount of intraretinal hemorrhage can also be noted. B, Optical coherence tomogram of the left eye 2 months following intravitreous injection of triamcinolone acetonide shows resolution of macular edema. The central foveal thickness measured 100 µm.


The patient did well until 3 months following the injection, when his visual acuity decreased to 20/400. Macular edema was noted on slitlamp biomicroscopy, and foveal thickness was 500 µm on OCT. No further intervention was attempted at this point, and the patient has been observed with no change in his clinical status.


Comment

Triamcinolone acetonide is a corticosteroid that is commercially available, inexpensive, and commonly used as a periocular injection for the treatment of cystoid macular edema occurring secondary to uveitis or resulting from intraocular surgery. Intravitreous triamcinolone acetonide has been used experimentally in the prevention or treatment of proliferative vitreoretinopathy, retinal neovascularization, choroidal neovascularization, and most recently for macular edema secondary to diabetic retinopathy.2

In these 2 patients, we attempted to reduce macular edema secondary to CRVO by injecting triamcinolone acetonide into the vitreous cavity. Intravitreous injection of triamcinolone acetonide has been shown to have minimal adverse effects in both animal and clinical studies.3-4 Triamcinolone acetonide may reduce macular edema, possibly by reducing the breakdown of the blood-retinal barrier, nonspecifically inhibiting the arachadonic acid pathway, or downregulating vascular endothelial growth factor.

Intravitreous triamcinolone acetonide induced a prompt anatomic and functional improvement in our patient with nonischemic CRVO (case 1). The visual acuity of this patient improved from 20/200 to 20/25 in 1 month. Additionally, the thickness of the central fovea, as measured by OCT, was reduced from 600 µm to 100 µm in 1 month.

In the patient with ischemic CRVO (case 2), intravitreous triamcinolone acetonide also appeared to produce significant but temporary anatomic benefit. Visual acuity improvement was noted but was less dramatic than in the patient with nonischemic CRVO. As in the patient with nonischemic CRVO, the central foveal thickness was reduced rapidly and dramatically during 1 month following intravitreous injection. This effect, however, was transient; a decrease in visual acuity and an increase in macular edema occurred 3 months following injection. This may be related to the severity of ischemic CRVO. A single injection of triamcinolone acetonide may remain in the vitreous cavity for up to 3 months following injection.5 It is possible that 1 injection of intravitreous triamcinolone lasting 3 months in the vitreous cavity may be sufficient treatment for macular edema caused by nonischemic CRVO but not for macular edema caused by ischemic CRVO. A repeated injection might again have reduced the macular edema and improved visual acuity in the patient with ischemic CRVO.

In the absence of a definite role for macular laser photocoagulation in the setting of macular edema from CRVO, intravitreous injection of triamcinolone acetonide may be a viable treatment option. The 2 patients described previously had a prompt anatomic and functional response, although the need for repeated treatment and possible adverse effects should be investigated further. No adverse effects such as retinal detachment, endophthalmitis, cataract, or glaucoma occurred in this series. Further study is warranted to evaluate the safety and efficacy of this promising treatment modality for CRVO complicated by macular edema.


AUTHOR INFORMATION

Michael S. Ip, MD; K. S. Kumar, MD
Madison, Wis

Corresponding author and reprints: Michael S. Ip, MD, University of Wisconsin–Madison, Department of Ophthalmology and Visual Sciences, 600 Highland Ave, F4/336, Madison, WI 53792 (e-mail: msip{at}facstaff.wisc.edu).


REFERENCES

1. Evaluation of grid pattern photocoagulation for macular edema in central vein occlusion: the Central Vein Occlusion Study Group M report. Ophthalmology. 1995;102:1425-1433. ISI | PUBMED
2. Jonas JB, Sofker A. Intraocular injection of crystalline cortisone as adjunctive treatment of diabetic macular edema. Am J Ophthalmol. 2001;132:425-427. FULL TEXT | ISI | PUBMED
3. McCuen BW, Bessler M, Tano Y, Chandler D, Machemer R. The lack of toxicity of intravitreally administered triamcinolone acetonide. Am J Ophthalmol. 1981;91:785-788. ISI | PUBMED
4. Danis RP, Ciulla TA, Pratt LM, Anliker W. Intravitreal triamcinolone acetonide in exudative age-related macular degeneration. Retina. 2000;20:244-250. FULL TEXT | ISI | PUBMED
5. Jonas JB, Hayler JK, Sofker A, Panda-Jonas S. Intravitreal injection of crystallinecortisone as an adjunctive treatment of proliferative diabetic retinopathy. Am J Ophthalmol. 2001;131:468-471. FULL TEXT | ISI | PUBMED

SECTION EDITOR: W. RICHARD GREEN, MD



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