Current intravitreal therapy and ocular hypertension

Abstract

To determine the effect of commonly used intravitreal agents on immediate and long-term IOP elevations and their association, if any, with glaucoma. Literature searches in PubMed and the Cochrane databased in January 2020 yielded 407 individual articles. Of these, 87 were selected for review based on our inclusion criteria. Based on the evidence provided, 20 were assigned level I, 27 level II, and 22 level III. Eight articles were rejected because of poor quality, insufficient clarity, or irrelevance based on standardized protocols set out by the American Academy of Ophthalmology. The studies that reported on short-term IOP elevation (i.e., between 0 and 60 min) showed that an immediate increase in IOP is seen in all patients who receive anti-VEGF agents or triamcinolone acetonide when measured between 0 and 30 min of intravitreal injection and that the IOP elevation decreases over time. The data on long-term IOP elevation were mixed; Pretreatment with glaucoma medications, anterior chamber tap, vitreous reflux, longer intervals between injections, and longer axial lengths were associated with lower IOP elevations after injection of anti-VEGF agents, while the position of the implant vis-à-vis, the anterior chamber was important for steroid therapy. Data were mixed on the relationship between IOP increase and the type of intravitreal injection, number of intravitreal injections, preexisting glaucoma, and globe decompression before injection. There were no data on the onset or progression of glaucoma in the studies reviewed in this assessment. However, some studies demonstrated RNFL thinning in patients receiving chronic anti-VEGF therapy. Most, if not all, intravitreal agents cause ocular hypertension, both in the short term and long term. The functional consequences of these observations are not very clear.

Influence of Chronic Ocular Hypertension on Emmetropia: Refractive, Structural and Functional Study in Two Rat Models

“…When ocular hypertension occurs in older ages, scleral tissues are more rigid and stiffen [55], explaining the greater glaucomatous damage (IOP spikes are more poorly mitigated by less elastic sclera), the outward shift of the lamina cribosa and remodeling of connective tissue [56], and the deeper anterior chamber described in both the ES model and DBA/2J glaucomatous mice (not observed in OHT models using cauterization, probably due to the experimental intervention itself) [57,58]. Indeed, there is increasing evidence about the development of delayed and sustained OHT associated with repeated intravitreal anti-vascular endothelial growth factor injections in retinal diseases, such as age-related macular degeneration [59,60]. Several structure optic nerve head manifestations after intravitreal volume injections have been lately described as a mechanical displacement of the optic nerve head and canal expansion, with a widening and deepening of the optic, a prelaminar tissue thinning and a Bruch membrane opening expansion, suggesting structural changes after IOP and volume increase in aged patients, with rigid sclera [61].…”

Intra-Ocular Pressure Response to Dexamethasone Implant Injections in Patients with a History of Filtering Surgery: The TRABEX Study

“…OHT resulting from DEX-I intravitreal injections is usually successfully managed with IOP-lowering therapy [3,4]. However, some cases of high-responders have been reported with DEX-I, with an increase in IOP of more than 15 mmHg according to Becker's classification [2,8,9]. Steroid-induced OHT results from the inhibition of proteases and phagocytosis of the trabecular cells, which reduces damage to the extracellular matrix of the trabecular meshwork [10,11].…”

Intraocular pressure: Focus on corticosteroids

“…Sudhalkar and colleagues comprehensively reviewed intraocular pressure (IOP) profile of intravitreal drugs. [ 1 ] The undisputed elephant in the room is intravitreal corticosteroid; and in the Indian context, triamcinolone acetonide (IVTA), which merits further discussion:…”