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Brusini, P.; Tosoni, C.; Zeppieri, M. Canaloplasty in Corticosteroid-Induced Glaucoma. Encyclopedia. Available online: https://encyclopedia.pub/entry/43157 (accessed on 27 July 2024).
Brusini P, Tosoni C, Zeppieri M. Canaloplasty in Corticosteroid-Induced Glaucoma. Encyclopedia. Available at: https://encyclopedia.pub/entry/43157. Accessed July 27, 2024.
Brusini, Paolo, Claudia Tosoni, Marco Zeppieri. "Canaloplasty in Corticosteroid-Induced Glaucoma" Encyclopedia, https://encyclopedia.pub/entry/43157 (accessed July 27, 2024).
Brusini, P., Tosoni, C., & Zeppieri, M. (2023, April 18). Canaloplasty in Corticosteroid-Induced Glaucoma. In Encyclopedia. https://encyclopedia.pub/entry/43157
Brusini, Paolo, et al. "Canaloplasty in Corticosteroid-Induced Glaucoma." Encyclopedia. Web. 18 April, 2023.
Canaloplasty in Corticosteroid-Induced Glaucoma
Edit

Canaloplasty should be considered as a possible alternative to filtering surgery in this form of glaucoma when medical therapy is not sufficient to maintain the intraocular pressure (IOP) within reasonable limits.

canaloplasty non-perforating surgical procedures corticosteroid-induced glaucoma

1. Introduction

Corticosteroid-induced glaucoma is a quite common form of secondary glaucoma due to either systemic or, more frequently, topical, peri- or intraocular administration of glucocorticoids in predisposed subjects [1][2][3][4][5]. It is known that corticosteroids raise intraocular pressure (IOP) by lowering the facility of aqueous outflow. Quite a high percentage of normal subjects (ranging from 5% to over 40% depending on the definition of corticosteroid-responders [6][7] may undergo a significant increase of IOP after using topical corticosteroids for several days. The increasing use of intravitreal injections of triamcinolone acetonide and intravitreal implants of dexamethasone for exudative maculopathies will probably exacerbate this problem. Secondary glaucoma can develop in some cases, even though for most patients the IOP returns to baseline after ceasing steroid use. If traditional medical therapy is not able to lower IOP within the safe range, structural and functional damage can quickly develop. In these cases, a laser trabeculoplasty can be attended [8][9][10], but more often a surgical treatment must be performed before serious visual impairment occurs. Trabeculectomy with intra-operative antimetabolites is still considered to be the gold standard surgical procedure for different types of glaucoma, including corticosteroid-induced glaucoma [11][12]. This technique is simple to perform and effective, however, several early and late potentially serious complications can occur. In particular, problems related to the subconjunctival bleb, and the frequent development of a cataract can be particularly disturbing in young patients, who are often the subjects that develop corticosteroid-induced glaucoma.
Canaloplasty is a non-perforating bleb-less technique, introduced some years ago, in which a 10-0 prolene suture is positioned and tensioned within Schlemm’s canal, previously dilated with a viscoelastic agent, thus facilitating aqueous outflow through natural pathways [13][14].

2. Preliminary Results for Canaloplasty in Corticosteroid-Induced Glaucoma

Surgery is sometimes needed to control ocular hypertension and delay damage progression in patients with corticosteroid-induced glaucoma, especially considering that visual field defect progression can be fast and severe if IOP is very high. However, unlike patients with primary open-angle glaucoma or pseudoexfoliation glaucoma, which often show advanced visual field loss, patients with corticosteroid-induced glaucoma usually have normal optic nerves and visual fields at the beginning. For this reason, an IOP in the mid-teens is usually adequate in order to avoid any structural and/or functional damage. In this type of patient, even with very high pre-operative IOP levels, non-filtering surgical procedures, such as goniotomy [15], trabeculotomy [16][17][18][19], trabecular stents [20], viscocanalostomy [21] or deep sclerectomy [22] may be an interesting option, even if they are less effective than trabeculectomy in lowering IOP, considering the lower risk of complications. Nowadays, canaloplasty should be considered as a step ahead of these procedures with very interesting long-term outcomes in various forms of open-angle glaucoma [23][24][25][26][27].
The mid-term results in a small cohort of patients with corticosteroid-induced glaucoma unresponsive to medical therapy appear to be particularly good in comparison with other types of glaucoma, where the mean IOP usually ranges between 15 and 17 mmHg, with a percentage of success after one year ranging between 60% and 95%, depending on the definition of success used [14][23][24][25][26][27]. In particular, if a cut-off of ≤ 16 mmHg is taken in order to define successful cases, the percentage of qualified success reported in the literature is about 50% in comparison with the 100% obtained in the researchers' nine cases.
The reasons for this favorable behavior are probably various and include: (1) histopathologic studies in corticosteroid-induced glaucoma demonstrated an increased density of the cribriform meshwork and thinning of the endothelial lining of Schlemm’s canal [28][29]; in cases of elevated IOP, a collapse of aqueous plexus and collector channel ostia obstructed by herniation was observed in bovine eyes [30], resulting in a decrease in the effective filtration area. Canaloplasty is able to overcome this obstacle, allowing the restoration of the aqueous humor outflow; (2) patients with this type of glaucoma are usually relatively young with well-functioning aqueous humor pathways, which is a fundamental requirement to obtain satisfactory results after canaloplasty; (3) all of the patients were under medical therapy for a short period before the operation; it is well known that topical therapy for glaucoma has negative effects in all glaucoma surgeries.
It should be noted, however, that the percentage of patients who require pharmacological therapy, even at a lower dosage, to maintain adequate IOP control seems to increase with time.
The study is currently still underway. New patients with corticosteroid-induced glaucoma that fit the inclusion criteria are being added and follow-up data of existing patients are being constantly updated to provide long-term results and a larger cohort for future study. Regarding these patients, multicentric randomized studies with a larger population, where canaloplasty is compared to gold-standard surgery (trabeculectomy), are needed to draw more definite and robust conclusions.

3. Conclusions

Canaloplasty is a very promising surgical technique in eyes with high IOP, which is usually the case in patients with corticosteroid-induced glaucoma. In the small cohort of patients, postoperative IOP was able to be maintained within physiological values, even if some medical therapy is occasionally still required. Considering that ocular hypertension is the main risk factor for structural and functional damage in corticosteroid-induced glaucoma, target IOP may not need to be very low to avoid the onset or progression of the damage. Even if the sample taken into consideration in the study was limited, the good outcomes and the low rate of complications observed with this non-perforating procedure are very encouraging and could entice glaucoma specialists to consider early surgical treatment in the management of this kind of patient.

References

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  2. Kersey, J.P.; Broadway, D.C. Corticosteroid-induced glaucoma: A review of the literature. Eye (Lond.) 2006, 20, 407–416.
  3. Kiddee, W.; Trope, G.E.; Sheng, L.; Beltran-Agullo, L.; Smith, M.; Strungaru, M.H.; Baath, J.; Buys, Y.M. Intraocular pressure monitoring post intravitreal steroids: A systematic review. Surv. Ophthalmol. 2013, 58, 291–310.
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  5. Mazzarella, S.; Mateo, C.; Freixes, S.; Burés-Jelstrup, A.; Rios, J.; Navarro, R.; García-Arumí, J.; Corcóstegui, B.; Arrondo, E. Effect of intravitreal injection of dexamethasone 0.7 mg (Ozurdex®) on intraocular pressure in patients with macular edema. Ophthalmic Res. 2015, 54, 143–149.
  6. Armaly, M. Effects of corticosteroids on intraocular pressure and fluid dynamics I. The effect of dexamethasone in normal subject. Arch. Ophthalmol. 1963, 70, 482–491.
  7. Becker, B. Intraocular pressure response to topic corticosteroids. Investig. Ophthalmol. Vis. Sci. 1965, 4, 198–205.
  8. Pizzimenti, J.J.; Nickerson, M.M.; Pizzimenti, C.E.; Kasten-Aker, A.G. Selective laser trabeculoplasty for intraocular pressure elevation after intravitreal triamcinolone acetonide injection. Optom. Vis. Sci. 2006, 83, 421–425.
  9. Rubin, B.; Taglienti, A.; Rothman, R.F.; Marcus, C.H.; Serle, J.B. The effect of selective laser trabeculoplasty on intraocular pressure in patients with intravitreal steroid-induced elevated intraocular pressure. J. Glaucoma 2008, 17, 287–292.
  10. Tokuda, N.; Inoue, J.; Yamazaki, I.; Matsuzawa, A.; Munemasa, Y.; Kitaoka, Y.; Takagi, H.; Ueno, S. Effects of selective laser trabeculoplasty treatment in steroid-induced glaucoma. Nippon Ganka Gakkai Zasshi 2012, 116, 751–757. (In Japanese)
  11. Ang, M.; Ho, C.L.; Tan, D.; Chan, C. Severe vernal keratoconjunctivitis requiring trabeculectomy with mitomycin C for corticosteroid-induced glaucoma. Clin. Exp. Ophthalmol. 2012, 40, e149–e155.
  12. Fitzgerald, J.T.; Saunders, L.; Ridge, B.; White, A.J.; Goldberg, I.; Clark, B.; Mills, R.A.; Craig, J.E. Severe intraocular pressure response to periocular or intravitreal steroid treatment in Australia and New Zealand: Data from the Australian and New Zealand Ophthalmic Surveillance Unit. Clin. Exp. Ophthalmol. 2015, 43, 234–238.
  13. Koerber, N. Canaloplasty—A new approach to nonpenetrating glaucoma surgery. Tech. Ophthalmol. 2007, 5, 102–106.
  14. Lewis, R.A.; von Wolff, K.; Tetz, M.; Korber, N.; Kearney, J.R.; Shingleton, B.; Samuelson, T.W. Canaloplasty: Circumferential viscodilation and tensioning of Schlemm's canal using a flexible microcatheter for the treatment of open-angle glaucoma in adults. Interim clinical study analysis. J. Cataract. Refract. Surg. 2007, 33, 1217–1226.
  15. Choi, E.Y.; Walton, D.S. Goniotomy for steroid-induced glaucoma: Clinical and tonographic evidence to support therapeutic goniotomy. J. Pediatr. Ophthalmol. Strabismus 2015, 52, 183–188.
  16. Kawamura, M.; Zako, M. Successful trabeculotomy in a patient with corticosteroid-induced glaucoma with anti-aquaporin 4 antibody-positive neuromyelitis optica: A case report. J. Med. Case Rep. 2013, 7, 101.
  17. Iwao, K.; Inatani, M.; Tanihara, H. Japanese Steroid-Induced Glaucoma Multicenter Study Group. Success rates of trabeculotomy for steroid-induced glaucoma: A comparative, multicenter, retrospective cohort study. Am. J. Ophthalmol. 2011, 151, 1047–1056.
  18. Dang, Y.; Kaplowitz, K.; Parikh, H.A.; Roy, P.; Loewen, R.T.; Francis, B.A.; Loewen, N.A. Steroid-induced glaucoma treated with trabecular ablation in a matched comparison with primary open-angle glaucoma. Clin. Exp. Ophthalmol. 2016, 44, 783–788.
  19. Ngai, P.; Kim, G.; Chak, G.; Lin, K.; Maeda, M.; Mosaed, S. Outcome of primary trabeculotomy ab interno (Trabectome) surgery in patients with steroid-induced glaucoma. Medicine (Baltim.) 2016, 95, e5383.
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  22. Detry-Morel, M.; Escarmelle, A.; Hermans, I. Refractory ocular hypertension secondary to intravitreal injection of triamcinolone acetonide. Bull. Soc. Belg. Ophtalmol. 2004, 292, 45–51.
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  24. Lewis, R.A.; von Wolff, K.; Tetz, M.; Koerber, N.; Kearney, J.R.; Shingleton, B.J.; Samuelson, T.W. Canaloplasty: Three-year results of circumferential viscodilation and tensioning of Schlemm canal using a microcatheter to treat open-angle glaucoma. J. Cataract. Refract. Surg. 2011, 37, 682–690.
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  28. Kayes, J.; Becker, B. The human trabecular meshwork in corticosteroid-induced glaucoma. Trans. Am. Ophthalmol. Soc. 1969, 67, 339–354.
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  30. Battista, S.A.; Lu, Z.; Hofmann, S.; Freddo, T.; Overby, D.R.; Gong, H. Reduction of the available area for aqueous humor outflow and increase in meshwork herniations into collector channels following acute IOP elevation in bovine eyes. Investig. Ophthalmol. Vis. Sci. 2008, 49, 5346–5352.
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