Journals / Middle Black Sea Journal of Health Science / 2018 / Cilt: 4 - Sayı: 1

Ocular Hypertension and Glaucoma after Intravitreal Injection of Triamcinolone Acetonide

Pages
24–30
Publication Date
2018-04-20
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

However, the risk of glaucoma requiring surgery or long term antiglaucomatous use validate the necessity of a meticulous patient selection and close monitorization of IOP.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: The use of intravitreal triamcinolone acetonide (IVTA) for intraocular neovascular, proliferative and edematous diseases has led to an increased incidence of corticosteroid-induced ocular hypertension.
📊
Key Findings & Data:Even though largely replaced with anti-vascular endothelial growth factor (anti-VEGF) agents and slow-release dexamethasone implants, boosters are still required in nonresponsive or minimally responsive patients, in cases of tachyplaxis to these agents, or in combination therapies with anti-VEGFs.Metods: The records of 136 eyes of 124 patients who underwent 4 mg/ml IVTA treatment for macular edema of variable etiologies of diabetic macular edema, retinal vein occlusions, subretinal choroidal neovascularization, Irvine-Gass Syndrome, retinitis pigmentosa and idiopathic juxtafoveal telengiectasia in the period 2001–2006 were reviewed.
💡
Conclusion & Impact:However, the risk of glaucoma requiring surgery or long term antiglaucomatous use validate the necessity of a meticulous patient selection and close monitorization of IOP.
🔬Design:Review & Systematic Survey
📍Scope:2001–2006 Verileri
⚙️Variables:intravitreal triamcinolone acetonide · streoid induced glaucoma · macular edema

Abstract

Objective: The use of intravitreal triamcinolone acetonide (IVTA) for intraocular neovascular, proliferative and edematous diseases has led to an increased incidence of corticosteroid-induced ocular hypertension. Even though largely replaced with anti-vascular endothelial growth factor (anti-VEGF) agents and slow-release dexamethasone implants, boosters are still required in nonresponsive or minimally responsive patients, in cases of tachyplaxis to these agents, or in combination therapies with anti-VEGFs.Metods: The records of 136 eyes of 124 patients who underwent 4 mg/ml IVTA treatment for macular edema of variable etiologies of diabetic macular edema, retinal vein occlusions, subretinal choroidal neovascularization, Irvine-Gass Syndrome, retinitis pigmentosa and idiopathic juxtafoveal telengiectasia in the period 2001–2006 were reviewed. Seventy-six eyes of 71 patients of which were followed for at least 3 months were included in the study. The patients were examined at the first day, second week, first month and every month after the injection. Mean intraocular pressure (IOP), IOP exceeding 21 mmHg and percentage of patients exhibiting IOP increase of 5 mmHg after IVTA injection, during the follow-up period were evaluated and compared statistically. Results: Mean age was 56.64±12.65 years and male to female ratio was 35/36. Mean follow-up time was 12.13±10.30 months. The mean IOP increased statistically (p= <0.001) during follow-up from 14.95±3.15 mmHg pre-injection level reaching to a maximum of 21.66±6.48 mmHg and decreased statistically (p= <0.001) to 15.58±4.16 mmHg at the end of the follow-up. There was no statistical difference between pre-injection and post-injection IOP levels (p=0.406). The IOP levels exceeded 21 mmHg in 46.05% of the eyes. There was an increase of 5 mmHg and more above the pre-injection level in the 53.94% of the eyes. Maximum IOP levels were reached at the 2.77±3.72 month. In 24 (31.58%) eyes, topical antiglaucomatous therapy was needed and later 1 eye (4.6%) required surgical intervention and 1 eye (4.6%) required argon laser trabeculoplasty to lower the IOP. Conclusion: The most common complication following İVTA injections is rise in IOP. Most of these ocular hypertension cases are controllable by medical therapy. However, the risk of glaucoma requiring surgery or long term antiglaucomatous use validate the necessity of a meticulous patient selection and close monitorization of IOP.

🔖

Cite This Article

KARAKAHYA, R. H., KALAYCI, D., KARAKURT, A. (2018). Ocular Hypertension and Glaucoma after Intravitreal Injection of Triamcinolone Acetonide. Middle Black Sea Journal of Health Science, Cilt: 4 - Sayı: 1, 24–30. https://ajindex.com/articles/791218

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (14)

  1. Agrawal S, Agrawal J, Agrawal T. Management of intractable glaucoma following intravitreal triamcinolone acetonide. Am J Ophthalmol 2004; 138: 286–287.
  2. Becker B, Bresnick G, Chevrette L, et al. Intraocular pressure and its response to topical corticosteroids in diabetes. Arch Ophthalmol 1966; 76: 477–483.
  3. Breusegem C, Vandewalle E, Van Calster J, et al. Predictive value of a topical dexamethasone provocative test before intravitreal triamcinolone acetonide injection. Invest Ophthalmol Vis Sci 2009;50: 573–576.
  4. Ciardiella AP, Klancnik J,Schiff W,et al. Intravitreal triamcinolone for the treatment of refractory diabetic macular oedema with hard exudates: an optical coherence tomography study. Br J Ophthalmol 2004;88:1131-6
  5. Clark AF, Wordinger RJ: The role of steroids in outflow resistance. Exp Eye Res 2009; 88: 752–759.
  6. Çekiç O, Chang S, Tseng JJ, et al. Intravitreal triamcinolone treatment for macular edema associated with central retinal vein occlusion and hemiretinal vein occlusion. Retina 2005; 25: 846-850.
  7. Gillies MC, Simpson JM, Billson FA, et al. Safety of an intravitreal injection of triamcinolone: results from a randomized clinical trial. Arch Ophthalmol 2004; 122:336–340.
  8. Holekamp NM, Thomas MA, Pearson A. The safety profile of long-term, high-dose intraocular corticosteroid delivery. Am J Ophthalmol. 2005 Mar;139(3):421-8.
  9. Jonas JB, Kreissig I, Degenring R. Intraocular pressure after intravitreal injection of triamcinolone acetonide. Br J Ophthalmol 2003;87:24-27
  10. Jonas JB, Harder B, Kamppeter BA. Inter-eye difference in diabetic macular edema after unilateral injection of triamcinolone acetonide. Am J Ophthalmol 2004a;138:970-77.
  11. Jonas JB, Degenrig RF, Kamppeter BA,et al.Duration of the effect of Intravitreal triamcinolone acetonide.as treatment for diffuse diabetic macular edema. Am J Ophthalmol 2004b;138:158-160. Jonas JB. Intravitreal triamcinolone acetonide for treatment of intraocular oedematous and neovascular diseases. Acta Ophthalmol Scand 2005;83(6): 645-63.
  12. Jonas JB, Akkoyun I,Kreissig I, Degenring RF. Diffuse diabetic macular edema treated by intravitreal triamcinolone acetonide: a comparative nonrandomized study. Br JOphthalmol 2005a:89:321-326.
  13. Jonas JB, Akkoyun I, Kamppeter B, et al. Branch retinal vein occlusion treated by intravitreal triamcinolone acetonide. Eye 2005b;19:65-71.
  14. Jonas JB, Degenring RF, Kreissig I, Akkoyun I, Kamppeter BA. Intraocular pressure elevation after intravitreal triamcinolone acetonide injection. Ophthalmo