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Journal of Vitreoretinal Diseases logoLink to Journal of Vitreoretinal Diseases
. 2025 Aug 20:24741264251365386. Online ahead of print. doi: 10.1177/24741264251365386

Intraocular Pressure Outcomes Following Suprachoroidal Triamcinolone Acetonide in Patients With Glaucoma, Ocular Hypertension, or Steroid Response

Nicholas R Bello 1, Robert C Wang 2, Joseph Boss 3,4, Michael Singer 5, Sophia Hopkins 3, Kiran Billawala 6, Christopher R Henry 6, Danny A Mammo 1,
PMCID: PMC12367709  PMID: 40852329

Abstract

Purpose: To examine the effect of suprachoroidal triamcinolone acetonide on intraocular pressure (IOP) in patients with a known history of glaucoma, ocular hypertension, or steroid response. Methods: This was a multicenter, retrospective cohort study examining patients with glaucoma, ocular hypertension, or a prior steroid response who received suprachoroidal triamcinolone acetonide between February 1, 2022, and December 31, 2023. Patient charts were reviewed to record IOP at the time of treatment with suprachoroidal triamcinolone acetonide and at follow-up. Results: Ten (17%) of 59 eyes experienced an IOP increase of 5 mm Hg or greater following suprachoroidal triamcinolone acetonide injection. At follow-up, 3 eyes (5%) were documented to have an IOP of greater than 25 mm Hg, and no eyes were found to have an IOP greater than 35 mm Hg. Notably, 30 (79%) of 38 eyes with a prior steroid response did not develop an IOP elevation of 5 mm Hg or higher. When removing eyes that had prior incisional glaucoma surgery, 17 (68%) of 25 eyes with prior steroid response still did not develop an IOP elevation of 5 mm Hg or greater. No eyes in this study required glaucoma surgery following suprachoroidal triamcinolone acetonide within the follow-up period. The mean follow-up from initial suprachoroidal triamcinolone acetonide to first visit was 42.0 days. Conclusions: This study examined patients who would be considered high-risk for intraocular steroid therapy. In this population, there was a lower tendency to have an IOP response following suprachoroidal triamcinolone acetonide compared with published rates of IOP elevation from intraocular steroids in eyes without a known steroid response. All patients receiving local corticosteroids should be monitored for IOP elevations.

Keywords: glaucoma, intraocular pressure, noninfectious uveitis, ocular hypertension, steroid response, suprachoroidal triamcinolone acetonide

Introduction

Ophthalmologists can choose from a variety of corticosteroid options to treat macular edema from noninfectious uveitis. 1 Topical, periocular, and intraocular corticosteroids can effectively treat uveitic macular edema.25 Intraocular corticosteroid delivery has been shown to be more effective than periocular delivery, but it is associated with an increased risk of intraocular pressure (IOP) rise, a known adverse effect of corticosteroids. 6 Increased IOP can lead to or exacerbate preexisting glaucoma; therefore, ophthalmologists may be hesitant to use long-term steroid delivery medications in patients with preexisting glaucoma, ocular hypertension, or prior steroid response.7,8 The prescribing label for the intravitreal dexamethasone implant lists advanced glaucoma as a contraindication to use. 9 The prescribing labels for the injectable 0.18 mg fluocinolone acetonide implant and the suprachoroidal triamcinolone acetonide injectable suspension list increased IOP and glaucoma as warnings and precautions.10,11

Suprachoroidal triamcinolone acetonide (Bausch + Lomb) was approved as a new therapeutic option in October 2021 after it demonstrated efficacy in treating uveitic macular edema. In the MAGNOLIA and PEACHTREE trials, the IOP increases in the study populations were less than those seen in studies of intravitreal dexamethasone and intravitreal fluocinolone acetonide implants.2,1214 Whether or not this decreased IOP response is seen in the real world is not yet established. Given that patients with uveitic macular edema and a history of IOP issues present treatment risks, more data are needed to determine if certain available therapeutic options may be safer in these patients. Our study examined the effect of suprachoroidal triamcinolone acetonide on IOP in patients with a known history of glaucoma, ocular hypertension, or steroid response.

Methods

This was a multicenter, retrospective study of patients treated with suprachoroidal triamcinolone acetonide at the Cole Eye Institute, Cleveland Clinic (Cleveland, OH), Texas Retina Associates (Dallas, TX), Retina Specialists of Michigan (Grand Rapids, MI), Medical Center Ophthalmology Associates (San Antonio, TX), and Retina Consultants of Texas (Houston, TX). This retrospective study was approved by the institutional review boards at each study site. The study and data accumulation conformed with all country, federal, or state laws, and the study adhered to the tenets of the Declaration of Helsinki.

All consecutive patients who received suprachoroidal triamcinolone acetonide between February 1, 2022, and December 31, 2023, were identified by the performing physicians. All patients received suprachoroidal triamcinolone acetonide for uveitic macular edema. Patient charts were reviewed to record IOP at the time of treatment with suprachoroidal triamcinolone acetonide and at follow-up visits. Method of IOP collection was not standardized and included applanation, TonoPen (Medtronic), and iCare. Demographic information as well as the type of noninfectious uveitis and details regarding glaucoma, ocular hypertension, or steroid response diagnoses were documented for each patient. In the case of prior steroid response, charts were reviewed to identify the causative agent (topical, periocular or intraocular injection, or oral corticosteroid), IOP increase, and IOP-lowering drops used. Glaucoma was defined as either having a diagnosis from a comprehensive ophthalmologist or glaucoma specialist, or a cup-to-disc ratio greater than 0.6 combined with being on IOP-lowering medications. Ocular hypertension was defined as any previously recorded IOP greater than 21 mm Hg. A steroid response was defined as having an IOP increase greater than or equal to 5 mm Hg with any prior corticosteroid use. In addition, lens status and previous intraocular surgeries were recorded. It was noted whether these medical or surgical interventions occurred prior to, concurrent with, or after suprachoroidal triamcinolone acetonide administration.

Patients without a history of glaucoma, ocular hypertension, or prior steroid response were excluded. Patients without follow-up or those who did not have a documented IOP at the time of suprachoroidal triamcinolone acetonide injection or at follow-up were also excluded. Data collection and statistical analysis were performed using Microsoft Excel (version 16.78). Demographic information was summarized using percentages. Measures of center and dispersion were described as mean and median with SD and range. Outcome measurements were evaluated using paired t tests with statistical significance determined by a P value < .05.

Results

Study Population Characteristics

Initially, 64 eyes were included in the study. Five eyes were excluded due to incomplete IOP data. Therefore, 59 eyes from 54 patients were analyzed in the study. Thirty-eight eyes (64%) were established steroid-responders. Seventeen eyes (29%) had undergone incisional glaucoma surgery (eg, tube shunt or trabeculectomy). Demographic information is summarized in Table 1. Fifty-three percent of eyes were from female patients. The average age at first injection was 67.9 ± 11.9 years. Sixty-five percent of eyes (38/59) had posterior or panuveitis. The most common noninfectious uveitis diagnoses were chronic post-operative inflammation (46%), idiopathic (34%), and birdshot chorioretinopathy (8%). It did not appear that there were any particular diagnoses with higher incidence of steroid response; however, our study is not adequately powered to make this claim. Most common IOP-related diagnoses were prior steroid response without glaucoma (39%), primary open-angle glaucoma (22%), other glaucoma (22%), and ocular hypertension (17%).

Table 1.

Study Population and Subgroup Information.

Number (%)
Subgroup All Eyes
(n = 59)
Eyes With Prior Steroid Response
(n = 38)
Eyes With Prior Steroid Response, Excluding Those With Prior Glaucoma Surgery
(n = 25)
Laterality
 Right 29 (49) 16 (42) 11 (44)
 Left 30 (51) 22 (58) 14 (56)
Sex
 Male 28 (47) 16 (42) 11 (44)
 Female 31 (53) 22 (58) 14 (56)
Race
 White 40 (68) 26 (68) 19 (76)
 Black 11 (19) 8 (21) 2 (8)
 Asian 1 (2) 0 (0) 0 (0)
Hispanic ethnicity 7 (12) 4 (11) 4 (16)
Uveitis location
 Anterior 12 (20) 5 (13) 4 (16)
 Intermediate 9 (15) 8 (21) 7 (28)
 Posterior 28 (47) 19 (50) 13 (52)
 Panuveitis 10 (17) 6 (16) 1 (4)
Lens status
 Aphakic 2 (3) 1 (3) 1 (4)
 Phakic 7 (12) 7 (18) 7 (28)
 Pseudophakic 50 (85) 30 (79) 17 (68)
Type of noninfectious uveitis
 Idiopathic 20 (34) 15 (39) 10 (40)
 Birdshot chorioretinopathy 5 (8) 5 (13) 5 (20)
 Vogt-Koyanagi-Harada disease 2 (3) 0 (0) 0 (0)
 Chronic Postoperative 27 (46) 14 (37) 7 (28)
 Nonparaneoplastic autoimmune retinopathy 3 (5) 2 (5) 1 (4)
 Inflammatory bowel disease–associated 1 (2) 1 (3) 1 (4)
 Tubulointerstitial nephritis and uveitis 1 (2) 1 (3) 1 (4)
Prior intraocular pressure issues
 Ocular hypertension 10 (17) 3 (8) 3 (12)
 Primary open-angle glaucoma 13 (22) 5 (13) 2 (8)
 Other glaucoma 13 (22) 7 (18) 3 (12)
 Prior steroid response without glaucoma 23 (39) 23 (61) 17 (68)

IOP Change From Suprachoroidal Triamcinolone Acetonide Injection to Follow-up

Mean IOP at the time of initial suprachoroidal triamcinolone acetonide injection was 14.4 mm Hg (SD, 4.0; median, 14; range, 7-24), and mean IOP at first follow-up was 15.6 mm Hg (SD, 5.7; median, 14; range, 7-33), a mean difference of 1.3 mm Hg (SD, 6.1; P = .12). The mean follow-up from initial suprachoroidal triamcinolone acetonide to first visit was 42.0 days (SD, 24.2; median, 36.5; range, 14-136). IOP change from suprachoroidal triamcinolone acetonide injection to first follow-up is summarized in Figure 1. Ten eyes (17%) experienced an IOP increase of 5 mm Hg or more at the first follow-up following suprachoroidal triamcinolone acetonide injection. None of the eyes that underwent a prior tube shunt or trabeculectomy procedure experienced an IOP rise of 5 mm Hg or greater. Figure 2 summarizes the observed IOP at first follow-up after suprachoroidal triamcinolone acetonide. One eye (1.7%) had an IOP between 26 and 30 mm Hg, 2 eyes (3.4%) had an IOP between 31 and 35 mm Hg, and 0 eyes had an IOP greater than 35 mm Hg.

Figure 1.

A scatter plot shows intraocular pressure change data.

IOP change from suprachoroidal triamcinolone acetonide injection to first follow-up (n = 59 eyes).

Abbreviation: IOP, intraocular pressure.

Figure 2.

The image is a bar chart displaying the intraocular pressure in mmHg for 59 eyes over a period.

Intraocular pressure at first follow-up following suprachoroidal triamcinolone acetonide (n = 59 eyes).

IOP-Lowering Medications and Procedures

Forty-four eyes (75%) were on topical IOP-lowering drops at the time of suprachoroidal triamcinolone acetonide injection. For these eyes, the mean number of IOP drops was 2.2 (range, 1-4). No eyes had IOP-lowering drops added to their medication regimen at the time of suprachoroidal triamcinolone acetonide injection. During the first follow-up, 11 (19%) of the 59 eyes were prescribed additional IOP-lowering drops. This includes 6 (60%) of the 10 eyes that had experienced an IOP elevation greater than 5 mm Hg. Five (33%) of the 15 eyes that were previously not on topical IOP-lowering drops were started on them at first follow-up. Among the entire study population, the mean number of IOP-lowering drops prior to initial suprachoroidal triamcinolone acetonide injection was 1.7 (range, 0-4). At first follow-up after suprachoroidal triamcinolone acetonide injection, the mean number of IOP-lowering drops was 1.9 (range, 0-4). No eyes underwent or were scheduled for glaucoma surgery or laser procedure in the follow-up period after receiving suprachoroidal triamcinolone acetonide.

Previous Corticosteroid Use

Fifty-eight (98%) of 59 eyes had trialed other corticosteroid therapies prior to treatment with suprachoroidal triamcinolone acetonide. Of these eyes, 38 (66%) were treated with prednisolone acetate, 33 (57%) with difluprednate, 21 (36%) with oral prednisone, 15 (26%) with an intravitreal dexamethasone implant, 13 (22%) with sub-Tenon triamcinolone acetonide, 7 (12%) with intravitreal triamcinolone acetonide, 5 (8%) with a surgical fluocinolone acetonide implant, and 4 (7%) with an injectable fluocinolone acetonide implant. At the time of suprachoroidal triamcinolone acetonide therapy, 5 eyes (8%) were still receiving oral prednisone, and 31 (53%) were receiving steroid eye drops.

Eyes With IOP Response to Any Prior Corticosteroid Use

Thirty-eight eyes (64%) were established steroid responders. In this subgroup, the causative agent of prior IOP response was difluprednate in 12 eyes (32%), surgical fluocinolone acetonide implant in 5 eyes (13%), intravitreal dexamethasone implant in 4 eyes (11%), prednisolone acetate in 3 eyes (8%), intravitreal triamcinolone acetonide in 3 eyes (8%), and an injectable fluocinolone acetonide implant in 2 eyes (5%). Mean IOP at the time of initial suprachoroidal triamcinolone acetonide injection in this subgroup was 15.1 mm Hg (SD, 4.2; median, 14.5; range, 7-24) and mean IOP at first follow-up was 16.3 mm Hg (SD, 6.0; median, 15; range, 7-33), with a mean difference of 1.2 mm Hg (SD, 6.3; P = .23). IOP change from suprachoroidal triamcinolone acetonide injection to first follow-up is summarized in Figure 3. In this subgroup, the mean time to follow-up from initial suprachoroidal triamcinolone acetonide injection to first visit was 38.0 days (SD, 19.1; median, 35.5; range, 14-105). At first follow-up, 8 eyes (21%) had an IOP increase of 5 mm Hg or more following suprachoroidal triamcinolone acetonide injection. One eye (2.6%) had an IOP between 25 and 30 mm Hg, 1 eye (2.6%) had an IOP between 31 and 35 mm Hg, and 0 eyes had an IOP greater than 35 mm Hg.

Figure 3.

This graph depicts intraocular pressure changes among patients, including those with steroid response to triamcinolone acetonide injections, as indicated by the legend specifying numbers for each category.

IOP change from suprachoroidal triamcinolone acetonide injection to first follow-up in patients with known steroid response (n = 38 eyes).

Abbreviation: IOP, intraocular pressure.

Of the 38 eyes with documented prior steroid-response, 13 eyes had incisional glaucoma surgery prior to receiving suprachoroidal triamcinolone acetonide. When examining the 25 remaining eyes with prior steroid response without previous incisional glaucoma surgery, the causative agent of prior IOP response was difluprednate in 6 eyes (24%), surgical fluocinolone acetonide implant in 4 eyes (16%), prednisolone acetate in 3 eyes (12%), intravitreal triamcinolone acetonide in 3 eyes (12%), and an intravitreal dexamethasone implant in 2 eyes (8%). Mean IOP at the time of initial suprachoroidal triamcinolone acetonide injection in this subgroup was 14.5 mm Hg (SD, 4.0; median, 14; range, 7-24), and mean IOP at first follow-up was 16.9 mm Hg (SD, 6.5; median, 15; range, 7-33), a mean difference of 2.4 mm Hg (SD, 6.8; P = .08). In this subgroup, the mean follow-up time from initial suprachoroidal triamcinolone acetonide administration to first visit was 38.7. days (SD, 21.4; median, 36; range, 14-105). At first follow-up, 8 eyes (32%) had an IOP increase of 5 mm Hg or more following suprachoroidal triamcinolone acetonide injection; 1 eye (4%) had an IOP between 25 and 30 mm Hg, 1 eye (4%) had an IOP between 31 and 35 mm Hg, and no eyes had an IOP greater than 35 mm Hg.

Conclusions

Macular edema is the leading cause of vision loss in patients with uveitis. 15 Treating recalcitrant uveitic macular edema in patients with a history of IOP response without corticosteroids presents limitations owing to the lower efficacy of steroid-sparing options. The treatment effect of intraocular steroids compared with periocular steroids such as sub-Tenon triamcinolone acetonide for uveitic macular edema has been well established, albeit with a higher-risk IOP profile. 6 Additionally, patients with glaucoma, ocular hypertension, or history of steroid response may already be on multiple topical drops to manage IOP, which can affect the ocular surface.16,17 In some cases, first-line treatment for uveitic macular edema includes topical drops, and adding more drops to a patient’s regimen can further affect the ocular surface and reduce compliance. 18

A literature review of 6015 intravitreal dexamethasone implant injections found that most studies demonstrate an IOP rise in 12% to 27% of all eyes. 8 Only 381 of these injections were in patients with noninfectious uveitis, and an IOP of more than 25 mm Hg was required to be considered a significant IOP rise. In patients being treated for noninfectious uveitis specifically, the incidence of an IOP increase of 5 mm Hg or higher after an intravitreal dexamethasone implant may be as high as 46%. 14 The injectable fluocinolone acetonide implant has been associated with an IOP increase of 5 mm Hg or more in 48% of patients with noninfectious uveitis. 13 Similarly, the surgical fluocinolone acetonide implant (Bausch + Lomb) has been implicated in causing an increase in IOP in as many as 65% of patients. 19 Additionally, the studies reviewed considered all patients, not just those at higher risk for IOP elevation, as examined in the current study. Early, small studies of suprachoroidal triamcinolone acetonide demonstrated significant improvement of macular edema without clinically meaningful increases in IOP or the need for IOP-lowering therapy.20,21 The PEACHTREE trial found more elevated IOP adverse events in the control group than the suprachoroidal triamcinolone acetonide group (15.6% vs 11.5%, respectively). 2 Given these data, the authors of the current study have cautiously used suprachoroidal triamcinolone acetonide in these higher-risk, harder-to-treat populations.

This report demonstrates a lower-than-expected incidence of IOP elevation following suprachoroidal triamcinolone acetonide in patients with a known history of glaucoma, ocular hypertension, or steroid response. At first follow-up, 10 (17%) of 59 eyes experienced an IOP increase of 5 mm Hg or more following suprachoroidal triamcinolone acetonide injection. Only 3 eyes (5%) were documented to have an IOP of greater than 25 mm Hg, and no eyes were found to have an IOP greater than 35 mm Hg. Notably, 79% of eyes with a prior steroid response did not develop an IOP elevation greater than 5 mm Hg. When removing prior steroid responders who had prior incisional glaucoma surgery, 68% of prior steroid responders still did not develop an IOP elevation greater than or equal to 5 mm Hg after suprachoroidal triamcinolone acetonide. No eyes in this study required scheduling for glaucoma surgery following suprachoroidal triamcinolone acetonide within the follow-up period.

Eleven of 59 eyes had IOP-lowering drops added at follow-up, and 0 eyes had IOP-lowering drops added at the visit when suprachoroidal triamcinolone acetonide was administered. Therefore, our results are not confounded by the IOP-lowering effect of topical medications. A recent meta-analysis noted a statistically significant increase in IOP 1 month after suprachoroidal triamcinolone acetonide injection but not at 3 and 6 months. 22 Given this information, the mean follow-up of 42 days and median of 36.5 days should be suitable to have captured a potential IOP elevation after administering suprachoroidal triamcinolone acetonide. The MEAD study, 23 a 3-year randomized sham-controlled trial of intravitreal dexamethasone implant in patients with diabetic macular edema, suggested a follow-up time of 6 to 8 weeks after injection to monitor IOP. Our mean 6-week follow-up is in line with this recommendation.

This study uniquely examined patients who would be considered high-risk for ocular steroid therapy. Despite the study population having a history of glaucoma, ocular hypertension, or steroid response, they demonstrated a lower tendency to have an IOP response than published rates in the general population receiving other forms of intraocular steroids (ie, intravitreal dexamethasone implant, injectable fluocinolone acetonide implant, and surgical fluocinolone acetonide implant). This remains true even when excluding subjects with prior incisional glaucoma surgery. Furthermore, those patients who did demonstrate an IOP response were able to get their IOP controlled with topical IOP-lowering therapy alone and did not require incisional glaucoma surgery or laser treatment during the study follow-up. This real-world, retrospective study is representative of a uveitis clinic that has patients with glaucoma, steroid response, or ocular hypertension, with and without prior incisional glaucoma surgery, providing valuable data to guide clinicians who see a wide range of patients with IOP concerns.

The mechanism is unclear, but the compartmentalization of suprachoroidal triamcinolone acetonide has been speculated to have less of an impact on the trabecular meshwork. 24 In rabbits, when comparing intravitreal triamcinolone acetonide with suprachoroidal triamcinolone acetonide, maximal concentrations of triamcinolone acetonide were significantly decreased in the vitreous humor, ciliary body, lens, and aqueous humor with suprachoroidal triamcinolone acetonide delivery compared with intravitreal. 25 Additionally, the expansion of the suprachoroidal space may influence either decreased aqueous production or increased uveoscleral outflow, or both. Further studies are needed to better understand the potential reduced IOP risks for this unique drug delivery method.

This study is limited by its sample size and retrospective design. Seventy-five percent of the study population was already on an IOP-lowering therapy, and 29% had previously undergone incisional glaucoma surgery. Mean follow-up was approximately 6 weeks and was variable, with an SD of 24.3 days. In some cases, this may have been too early to capture a potential rise in IOP. The study did not account for the distribution of patients across the participating centers and any potential differences in outcomes among these centers. IOP measurements were not standardized between practices with respect to measured technique. Possible confounders to IOP measurement, such as corneal thickness and time of measurement, were also not recorded in this study. Patient visual field data were not documented, and glaucoma stage was not recorded as the sites are primarily retina-specific practices.

This report demonstrates that IOP response was well-tolerated following suprachoroidal triamcinolone acetonide injection in many patients with noninfectious uveitis with comorbid glaucoma, ocular hypertension, or a prior steroid response. Clinicians should carefully consider patient-specific factors and weigh the risks and benefits when selecting intraocular steroids for noninfectious uveitis. Continued research will enhance our understanding of the comparative IOP responses among various treatment options, enabling more informed clinical decision-making. Regardless of delivery mechanism, all patients receiving local corticosteroid therapy should be continually monitored for IOP elevations.

Footnotes

Ethical Approval: This study was conducted in accordance with the Declaration of Helsinki. Approval was granted on July 16, 2024. The Institutional Review Board at the Cole Eye Institute acted as the central IRB, whose review was accepted by all participating institutions’ IRBs (Ref. 13-788).

Statement of Informed Consent: The central IRB determined that this research involved minimal risk and approved a waiver for informed consent.

The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of the article: Dr. Wang is a consultant to Bausch + Lomb, Genentech, Clearside, and EyePoint. Dr. Boss is a consultant to Alimera, Unity Biotechnology, and Bausch + Lomb. Dr. Singer is a consultant to Aerie, Biogen Bausch, Alimera, Adverum, Allergan, EyePoint, Genentech, Novartis, Ocular therapeutics, Regeneron, Unity, and Stealth; speaker for Allergan, Bausch, EyePoint, Genentech, Regeneron, Apellis, Iveric Bio, Biogen, and Cimerli; does contracted research for Aerie, Adverum, Allergan, Alimera, Apellis, Ashvanta, Clearside, DRCR, Genentech, Icon, Ionis, Iveric Bio, Kalvista, Kodiak, Jansen, Novartis, Ocuterra, Ocular Therapeutics, Opthea, Optos, Oysterpoint, Regeneron, Recens, Rezolute Medical, Santen, Senju, Sydnexis, Ribomic, Unity, and Valo; and has equity in Aviceda, Nanoscope, Olives, and Inflammasome. Dr. Henry is a consultant to Bausch + Lomb, EyePoint Pharmaceuticals, and Alimera Sciences. Dr. Mammo is a consultant to Bausch + Lomb, Alimera Sciences, and AbbVie, and a speaker for Apellis.

Funding: The authors received no financial support for the research, authorship, and/or publication of this article.

Data Availability Statement: The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.

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