Steroid Induced Glaucoma

From EyeWiki
(Redirected from Steroid induced Glaucoma)

Disease Entity

Steroid-induced ocular hypertension and steroid-induced glaucoma are elevated intraocular pressure (IOP), and glaucomatous optic neuropathy, respectively, which develop in the setting of corticosteroid use. This association was first appreciated in the 1950s, when Drs. Gordon and McLean described an increase in IOP caused by the systemic administration of adrenocorticotrophic hormone[1], and again several years later when Dr. Francois reported a case of elevated IOP after locally administered cortisone[2].

Since it was first reported, the definition of steroid-induced ocular hypertension has varied, but today is considered to be an IOP increase greater than 10 mm Hg from baseline. Patients who experience an IOP rise in the setting of glucocorticoid use are considered, “steroid responders”.

The timeline over which the IOP will rise depends on the potency of the glucocorticoid, the dose, as well as the route of administration. With topical steroid use, the IOP rise most commonly occurs between three to six weeks from initial use, and typically normalizes within two weeks of the cessation of therapy.[3] However, though three to six weeks is the most common time to see an IOP increase, patients can “respond” to steroids well after six weeks[4], and before three weeks, from initial use.[3] In one series, 2.8% of eyes that experienced an IOP elevation in the setting of steroid use, converted to glaucoma. Interestingly, all of these patients had a family history of glaucoma.[5] The duration of steroid treatment may play a role in the IOP elevation as well, as indicated by one study in which the IOP was found to remain elevated in patients being treated with steroid for more than four years.[6]


Steroid-induced glaucoma is a form of secondary open angle glaucoma in which aqueous outflow resistance is increased, leading to an elevation in IOP. This likely occurs through a number of mechanisms, including: induction of physical and mechanical changes in the microstructure of the trabecular meshwork (TM), inhibition of proteases and TM endothelial phagocytosis, and deposition of substance in the TM.[2]

One of the most marked changes to the microstructure of the TM induced by glucocorticoids involves the formation of cross-linked actin networks[7], and increased expression of myocilin[8], both of which have a significant effect on the cytoskeleton structure. Glucocorticoids have also been shown to increase expression of fibronectin,[9][10] and extracellular matrix deposition in the trabecular meshwork[11], which similarly increases aqueous outflow resistance.

Glucocorticoids bind to multiple receptors throughout the body, including glucocorticoid receptor alpha (GRalpha) and glucocorticoid receptor beta (GRbeta), which are ligand-activated transcription factors. GRbeta is thought to play a role in steroid resistance, and has been shown to block glucocorticoid responsiveness in TM cells, thereby suppressing phagocyctic activity.[12] This may lead to increased deposition of material such as debris and pigment in the juxtacanalicular meshwork of eyes with steroid induced glaucoma.[13][14]

It has also been postulated that actual physical obstruction by glucocorticoids themselves contributes to a reduction in aqueous outflow. This is based on the observation of white crystals in the angle in a patient who developed elevated IOP after intravitreal triamcinolone injection.[15]

Risk Factors

Anyone can be at risk for steroid induced glaucoma, and the risk of glaucoma increases as the duration of therapy increases.

A higher than average risk for steroid glaucoma is found in patients with:

  1. Primary open angle glaucoma (POAG)[16] [17]
  2. A first degree relative with POAG[18] [19]
  3. A history of previous steroid induced intraocular pressure (IOP) elevation
  4. Type 1 Diabetes Mellitus[20]
  5. Very young age (age less than six years old) or an older age[21]
  6. Connective tissue disease[22]
  7. Penetrating keratoplasty, especially in eyes with Fuchs endothelial dystrophy or keratoconus
  8. High myopia[23]

(Table 23.1 in Shields Textbook of Glaucoma, Sixth Ed. p. 346)

In this subset of patients, intraocular pressures should be monitored regularly. Care should be taken to avoid corticosteroids If possible. If corticosteroids are indicated, the judicious use of an adequate potency and duration should be considered.

Types of Steroids

Topical Ocular Preparations

IOP rise may occur with corticosteroid drops or ointment applied to the eye or with steroid preparations applied to the skin of the eyelids. In general, the potency of the steroid as well as the frequency and duration of use, appears to correlate with the risk of elevating the IOP.[24] For example, dexamethasone and prednisolone are more potent steroids and similarly increase the IOP more frequently than less potent steroids such as fluoromethalone, hydrocortisone, and rimexolone.[25]

Difluprednate (Durezol) is one of the most potent topical steroids, and one of the most likely to cause an increase in IOP. An estimated 3% of patients treated with difluprednate experience a significant increase in IOP. This estimate is based on a study of patients who had recently undergone ocular surgery and were treated with difluprednate two or four times daily in the post-operative period. Amongst the difluprednate group, 3% exhibited an increase in IOP 10 mm Hg or greater above their baseline to an IOP of 21 mm Hg or greater, compared to 1% in the placebo (vehicle only) group.[26] These findings were supported by another study of patients who underwent cataract surgery, which showed that 3.7% of those treated with difluprednate twice daily exhibited an IOP increase greater than 10 mm Hg or more from baseline to greater than 21 mm Hg, compared to 0% in the placebo group.[27]

Dexamethasone, prednisolone, and fluoromethalone are all early generation topical ocular corticosteroids. Because of their introduction prior to strict regulatory research requirements, placebo-controlled clinical trials are lacking.[28] The broadest comparative data comes from a small study which investigated the effect of multiple early generation topical corticosteroids on the IOP in ten known steroid responders. These patients underwent sequential testing with a number of topical steroids, including dexamethasone 0.005%, hydrocortisone 0.5%, fluoromethalone 0.1%, prednisolone acetate 1%, and dexamethasone 0.1%. Hydrocortisone 0.5% elicited the smallest IOP rise (average 3.2 mm Hg), followed by fluoromethalone 0.1% (average 6.1 mm Hg), dexamethasone 0.005% (average 8.2 mm Hg), and prednisolone 1.0% (average 10 mm Hg). Patients treated with dexamethasone 0.1% exhibited the greatest rise in IOP (average 22 mm Hg).[24]

As newer topical steroids have been released, comparative studies against earlier generation preparations, have provided greater insight into their efficacy and effect on IOP. In a study comparing the post-operative management of uneventful cataract surgery, the proportion of patients who displayed a significant increase in IOP (defined as a 6 mm Hg greater than preoperative IOP) was twice that in the difluprednate group compared to the prednisolone group (8% compared to 4.14%, respectively).[29] A study comparing the efficacy and safety of loteprednol with prednisolone acetate (each administered four times daily), found that the mean IOP and mean change in IOP was higher in patients treated with prednisolone, though this finding did not reach statistical significance.[30]

As displayed in the aforementioned studies, the potency of topical ophthalmic steroids tends to correlate with the severity of IOP rise. Ultimately, difluprednate is the most likely to elevate IOP, followed by dexamethasone, prednisolone, loteprednol, and fluoromethalone. However, the proportion of patients who will experience an IOP rise is not as well defined. As mentioned above, it is likely strongly correlated with patient risk factors for developing glaucoma regardless of steroid use, however, comparisons and incidence estimates in studies are confounded by non-modifiable glaucoma risk factors within the patient population as well as varying definitions of categorical IOP elevation.


This route of steroid delivery includes subconjunctival, sub-Tenon, and retrobulbar injections. The elevation in IOP noted cannot always be predicted by the patient’s response to topical steroid treatment,[31] however, the proportion of patients who experience an IOP response from periocular steroid is considerably greater than that of topical ophthalmic steroids. The IOP elevation after periocular steroids typically occurs after a few months, though can be seen within a week in early cases, and may return to baseline at the sixth to ninth month after injection.[32] In cases of IOP spikes after periocular steroid administration, it may be necessary to excise the depot of steroids in order to control the IOP. As a result, it can be useful to inject inferiorly as well as anteriorly when performing a subconjunctival or sub-Tenon’s injection.

Given the differing ocular pathology they are best used for, there are not many studies which offer direct comparison between periocular mechanisms of steroid delivery. Of the studies which compare routes of periocular steroid delivery, it appears that while all periocular steroids may increase IOP, the delivery route likely plays an important role in the timing to the peak effect, as well as how long this effect lasts. In one study on subconjunctival injection of repository corticosteroid, the mean peak in IOP occurred at 7.1 weeks, and lasted for a mean duration of 3 months.[33]

In a retrospective review primarily on the efficacy of retrobulbar versus sub-Tenons corticosteroid in treating pseudophakic cystoid macular edema (CME), the mean IOP peak was similar between the two groups (mean pretreatment IOP 14.1 mm Hg to peak IOP 17.7 mm Hg with sub-Tenon, mean pretreatment IOP 15.1 mm Hg to peak IOP 17.6 mm Hg with retrobulbar). However, while the peak IOP occurred at a median of 1 month after treatment in the sub-Tenon steroid group, it occurred at a median of 10 months after treatment in the retrobulbar group, though the authors presumed this was likely due to the sub-tenon steroid administration as three injections at bi-weekly intervals.

Several studies offer comparisons between intravitreal and periocular delivery of corticosteroids. A study examining the efficacy of intravitreal and retrobulbar triamcinolone in patients with macular edema associated with branch retinal vein occlusion found an IOP increase in both therapy groups. However, the incidence of an IOP rise 20 mm Hg or greater was significantly higher in the intravitreal group (33.3%), compared to the retrobulbar group (7.4%). Although no significant difference in mean IOP throughout the follow-up period was appreciated, patients were only followed to three months before being re-treated.[34] Another study investigating the IOP elevation after intravitreal or sub-Tenons injection of triamcinolone found a statistically significant mean IOP elevation above baseline at all follow-up periods, though likely became clinically insignificant beyond 6 months. However, the mean IOP of eyes receiving sub-Tenon injection increased significantly at all follow-ups (1, 2, 3, 6 months), whereas the mean IOP of eyes receiving intravitreal injection was only significantly increased at the 1 month time point.[32]

All periocular steroids carry a risk of increasing IOP, though to different degrees. There aren’t many head-to-head comparisons between subconjunctival, sub-Tenons, and retrobulbar corticosteroid delivery to fully understand the risk comparison between the three. However, the proportion of those who receive periocular corticosteroids and experience an IOP elevation is likely greater than that with topical ophthalmic steroids, but less than that with intravitreal corticosteroids. In addition, the IOP elevation with periocular steroids is more likely to reach a peak months from the time of injection compared to intravitreal and topical steroids.


The most common corticosteroids administered intravitreally include triamcinolone, fluocinolone, and dexamethasone. Dexamethasone, often used at 0.4 mg or 0.8 mg dosing, is the more potent steroid, with a shorter duration of action. Triamcinolone is often dosed at 4 mg and has a duration of action extending to three months.[35] Most ocular pathology requiring treatment with intravitreal corticosteroids requires multiple treatments to maintain therapeutic effect, raising the risk of adverse events, such as endophthalmitis, as well as patient discomfort with multiple injections. For this reason, sustained release corticosteroid implants have an important role in the treatment of many ocular microvascular and inflammatory pathologies. Ozurdex is the shortest acting, and only biodegradable, sustained release implant, which is inserted into the vitreous where it releases dexamethasone at a controlled rate for up to 6 months. Retisert and Iluvien are non-biodegradable implants which release fluocinolone at a controlled rate for 30, and 36, months, respectively. Retisert is inserted pars plana and sutured to the sclera, whereas Iluvien is inserted pars plana into the vitreous.[35]

The timing and incidence rate of IOP elevation that develops after intravitreal administration of corticosteroids varies depending on the molecule and the dose. In about half of patients that received intravitreal triamcinolone, IOP elevation developed between two to four weeks after the injection. In eyes that are pseudophakic or have undergone vitrectomy, the rise can happen more rapidly.[36] [37] [38] In a systemic review of patients who had been treated with triamcinolone 4 mg, the onset of IOP elevation (defined as IOP of or greater than 21 mm Hg, or IOP of or greater than 10 mm Hg from baseline) was 2-4 weeks in randomized controlled trials and 1-8 weeks in non-randomized controlled trials.[39]

As mentioned, the incidence rate of IOP elevation varies according to the implant formulation. In the MEAD study, a randomized clinical trial of varying doses of dexamethasone implants, one third of patients in each implant group had a clinically significant increase in IOP necessitating treatment. None of these patients required implant removal, though one patient in each implant group (0.3%) did require incisional glaucoma surgery. Notably, this study found that the patients requiring IOP-lowering medications remained the same from year to year due to a lack of additional IOP increase after the first year, suggesting that there was no cumulative effect on IOP from the dexamethasone implant.[40] In a randomized clinical trial investigating the Retisert implant, elevated IOP was observed in 67% of patients, 5.8% of whom required filtering glaucoma surgery to manage IOP.[41] These rates are higher than those found in a randomized clinical trial investigating the Iluvien implant. The patients in this trial were divided into treatment groups according to dosage and amongst patients who received the lower dose (correlates with 0.19 mg Iluvien implant), 37.1% exhibited an IOP-related adverse event, and 4.8% required incisional glaucoma surgery.[42]

As indicated above, the incidence of IOP elevation associated with intravitreal corticosteroids appears to be directly correlated with the molecule and dose administered. Between the two fluocinolone implants, Retisert, which is inserted pars plana and sutured to sclera may carry a greater risk of IOP elevation.


Steroid induced glaucoma may develop after application of steroid preparations applied to the skin of the eyelids. This elevation occurs most frequently with chronic use, such as in patients with atopic dermatitis, and in patients with a family history of glaucoma.[43]

Close IOP monitoring of these patients is essential and consideration of a non-steroidal topical medication, such as tacrolimus and pimecrolimus, should be considered as an alternative in patients with glaucoma. Elevation in IOP has also been noted with application of steroids on skin that was not periocular, either from ocular contamination or systemic absorption. [44] Patients should be advised to wash their hands after applying dermatologic steroids or to use gloves.

Systemic and Non-Ocular Targeted

Steroids by mouth (PO) or intravenously (IV) have been shown to elevate IOP as well as, though less commonly so, non-ocular targeted localized steroids such as intranasal, inhaled,  and intraarticular.[45] The elevation appears to be correlated to the patient’s IOP response to topical steroids.[46][47]

An increase in IOP and glaucomatous change is a well-known risk of systemic corticosteroids for immunosuppression in the renal transplant patient population.[48][49] In a more recent study on pediatric inflammatory bowel patients treated with oral prednisone, 17 of the 54 patients (31.5%) were characterized as “steroid responders” (defined as IOP of 20 mm Hg or greater or a change in IOP of 6 mm Hg or greater, or a difference of 6 mm Hg or greater between the two eyes). Notably, in this group, when prednisone was reduced to 0-10 mg/day for 30 days or more, 7 patients showed a decrease in IOP of 6 mm Hg or greater.[50] Similar findings were uncovered in a large case-control study on elderly patients with new diagnoses of ocular hypertension or open angle glaucoma. This study found an adjusted odds ratio of having one of the aforementioned diagnosis, of 1.41 when comparing patients who used oral glucocorticoids with those who didn’t. Further, there was a dose-related increase in the adjusted odds ratio when categorized by 5-40 mg/day of hydrocortisone, 40-79 mg/day of hydrocortisone, and 80 mg/day or more of hydrocortisone.[51]

There is a relative paucity of large studies on the IOP effects of non-ocular targeted localized corticosteroids. In one cohort study based out of an orthopedic clinic, the IOP of patients receiving intraarticular knee injections of triamcinolone were compared to those receiving hyaluronic acid. This study showed a difference in the mean increase in IOP between the groups as well as a significant difference in the number of patients who developed an IOP increase > 7 mm Hg (29% in the triamcinolone group, 0% in the hyaluronic acid group)[52].

Several studies have explored the effect of intranasal steroids on IOP elevation.  One of the initial studies that raised a concern regarding IOP effects of intranasal corticosteroids was a case series of three patients with elevated IOP, thought to have developed after 3-5 months of beclomethasone intranasal spray.[45] More recent research has not produced similar findings, with multiple studies showing no significant change in IOP in all-comers, taking various preparations of intranasal corticosteroids.[53][54] However, in one study of patients already established with a glaucoma service, intranasal steroids were found to be associated with an increase in IOP, and a reduction in IOP upon removal.[55]

Multiple studies have shown that inhaled corticosteroids can increase the risk of IOP elevation, though as above, the evidence is strongest in patients with a personal or family history of glaucoma. One large, cross-sectional study found that inhaled corticosteroids were associated with a rise in IOP and magnification of glaucoma in patients who had a first-degree family history of glaucoma.[56]

Systemic corticosteroids carry a widely appreciated risk of ocular hypertension. However, as noted in the studies mentioned, there is a strong association between the risk of steroid response and the numerous non-modifiable risk factors associated with the development of glaucoma, namely a positive family history of glaucoma or pre-existing ocular hypertension or glaucoma in the patient themselves.


All patients receiving topical ocular steroids, periocular or intravitreal steroids need to be monitored regularly. Chronic ocular steroids should not be administered by non-ophthalmic physicians, unless patients are also being followed by an ophthalmologist. All patients using dermatologic steroids on the face should also have perioidic IOP measurements. Patients in the high risk groups mentioned above should use steroids judiciously and be monitored closely if the steroids are used long term.


Discontinue steroids—In the acute form of IOP elevation from steroids, discontinuing steroids can cause the IOP to normalize in days. In the chronic form, elevation of IOP can last one to four weeks[3], though if steroid therapy has been maintained for more than 18 months, the IOP can stay elevated far longer after withdrawal of therapy.[57] In a small subset of patients, the IOP may remain chronically elevated despite discontinuation of steroids.

Removal of depot steroids—One can cause a decrease in IOP by excising depot steroids.[36][38][58] For intravitreal steroids, vitrectomy can also be used to reduce IOP, however due to the need for ongoing steroid therapy to control underlying inflammation, many of these patients may require glaucoma medications or surgery to control IOP.[37]

Glaucoma treatment—Treatment of steroid-induced glaucoma is very similar to that for POAG, and includes the use of topical glaucoma medications, laser trabeculoplasty, filtering surgery, and glaucoma drainage implant surgery. Selective laser trabeculoplasty (SLT) has been proven to be effective in lowering IOP in patients with steroid-induced glaucoma by over 35% at one year[59], as well as preventing IOP spike in patients undergoing sub-tenon’s triamcinolone.[60]

Goniotomy is considered by some to be a particularly effective treatment in patients with steroid-induced glaucoma, with one small case series showing the achievement of surgical success in all patients who underwent goniotomy.[61] Similarly, canaloplasty has been proven to be a promising treatment for steroid-induced glaucoma, as indicated by a small cohort of patients who underwent this procedure, all of whom achieved complete success without serious complication.[62]


  1. Gordon, D. M., J. M. McLEAN, H. Koteen, F. P. Bousquet, W. D. McCUSKER, I. Baras, P. Wetzig, and E. W. D. Norton. 1951. “The Use of ACTH and Cortisone in Ophthalmology.” American Journal of Ophthalmology 34 (12): 1675–86.
  2. 2.0 2.1 Jones, Relief, 3rd, and Douglas J. Rhee. 2006. “Corticosteroid-Induced Ocular Hypertension and Glaucoma: A Brief Review and Update of the Literature.” Current Opinion in Ophthalmology 17 (2): 163–67.
  3. 3.0 3.1 3.2 Weinreb, R. N., J. R. Polansky, S. G. Kramer, and J. D. Baxter. 1985. “Acute Effects of Dexamethasone on Intraocular Pressure in Glaucoma.” Investigative Ophthalmology & Visual Science 26 (2): 170–75.
  4. Razeghinejad, M. Reza, and L. Jay Katz. 2012. “Steroid-Induced Iatrogenic Glaucoma.” Ophthalmic Research 47 (2): 66–80.
  5. François J. Corticosteroid glaucoma. Ann Ophthalmol. 1977;9(9):1075-1080.
  6. Espildora J, Vicuna P, Diaz E. Cortisone-induced glaucoma: a report on 44 affected eyes (in French). J Fr Ophthalmol. 1981;4(6-7):503-508.
  7. Clark, A. F., S. T. Miggans, K. Wilson, S. Browder, and M. D. McCartney. 1995. “Cytoskeletal Changes in Cultured Human Glaucoma Trabecular Meshwork Cells.” Journal of Glaucoma 4 (3): 183–88.
  8. Lo, Wayne R., Laura Leigh Rowlette, Montserrat Caballero, Ping Yang, M. Rosario Hernandez, and Teresa Borrás. 2003. “Tissue Differential Microarray Analysis of Dexamethasone Induction Reveals Potential Mechanisms of Steroid Glaucoma.” Investigative Ophthalmology & Visual Science 44 (2): 473–85.
  9. Johnson DH, Bradley JM, Acott TS. The effect of dexamethasone on glycosaminoglycans of human trabecular meshwork in perfusion organ culture. Invest Ophthalmol Vis Sci. 1990;31(12):2568-2571.
  10. Steely HT, Bowder SL, Julian MB, et al. The effects of dexamethasone on fibronectin expression in cultured human trabecular meshwork cells. Invest Ophthalmol Vis Sci.1992;33(7): 2242-2250.
  11. Johnson, D., J. Gottanka, C. Flügel, F. Hoffmann, R. Futa, and E. Lütjen-Drecoll. 1997. “Ultrastructural Changes in the Trabecular Meshwork of Human Eyes Treated with Corticosteroids.” Archives of Ophthalmology 115 (3): 375–83.
  12. Zhang, Xinyu, Cherie M. Ognibene, Abbot F. Clark, and Thomas Yorio. 2007. “Dexamethasone Inhibition of Trabecular Meshwork Cell Phagocytosis and Its Modulation by Glucocorticoid Receptor Beta.” Experimental Eye Research84 (2): 275–84.
  13. Rohen JW, Linner E, Witmer R. Electron microscopic studies on the trabecular meshwork in two cases of corticosteroid-glaucoma. Exp Eye Res.1973;17(1):19-31.
  14. Roll P, Benedikt O. Electron microscopic studies of the trabecular meshwork in corticosteroid glaucoma (in German). Klin Monatsbl Augenheilkd. 1979;174(3):421-428.
  15. Singh IP,Ahmad SI, Yeh D, et al. Early rapid rise in intraocular pressure after intravitreal triamcinolone acetonide injection. Am J Ophthalmol 2004;138(2)286-287.
  16. Armaly MF. Effect of corticosteroids on intraocular pressure and fluid dynamics I:the effect of dexamethasone in the normal eye. Arch Ophthalmol 1963;70:482-291.
  17. Armaly MF. Effect of corticosteroids on intraocular pressure and fluid dynamics II:the effect of dexamethasone in the glaucomatous eye. Arch Ophthalmol. 1963;70:492-499.
  18. Becker B, Hahn KA. Topical corticosteroids and heredity in primary open-angle glaucoma. Am J Ophthalmol 1964;54:543-551
  19. Davies TG. Tonographic survey of the close relatives of patients with chronic simple glaucoma. Br J Ophthalmol. 1968;52:32-39.
  20. Becker B. Diabetes mellitus and primary open-angle glaucoma. The xxvii Edwards Jackson memorial lecture. Am J Ophthalmol. 1971;1:1–16.
  21. Lam D SC, Dorothy F SP, Ng J SK et al. Ocular hypertensive and anti-inflammatory responses to different dosages of topical dexamethasone in children: a randomized trial. Clin Experiment Ophthalmol. 2005;33:252-258.
  22. Gaston, H, Absolon MJ, Thurtle, OA, Sattar, MA. Steroid responsiveness in connective tissue diseases. Br J Ophthalmo. 1983, 67:487-490.
  23. Podos SM, Becker B, Morton WR. High myopia and primary open-angle glaucoma. Am J Ophthalmol. 1966 Dec;62(6):1038-43. PubMed PMID: 5957877
  24. 24.0 24.1 Cantrill, H. L., P. F. Palmberg, H. A. Zink, S. R. Waltman, S. M. Podos, and B. Becker. 1975. “Comparison of in Vitro Potency of Corticosteroids with Ability to Raise Intraocular Pressure.” American Journal of Ophthalmology 79 (6): 1012–17.
  25. Sohn S,Hur W, Choi YR et al. Little evidence for association of the glaucoma gene MYOC with open angle glaucoma. Br J Ophthalmol 2010; 94:639-642.
  26. Korenfeld, Michael S., Steven M. Silverstein, David L. Cooke, Roger Vogel, Robert S. Crockett, and Difluprednate Ophthalmic Emulsion 0.05% (Durezol) Study Group. 2009. “Difluprednate Ophthalmic Emulsion 0.05% for Postoperative Inflammation and Pain.” Journal of Cataract and Refractive Surgery 35 (1): 26–34.
  27. Smith, Stephen, Douglas Lorenz, James Peace, Kimberly McLeod, R. S. Crockett, and Roger Vogel. 2010. “Difluprednate Ophthalmic Emulsion 0.05% (Durezol) Administered Two Times Daily for Managing Ocular Inflammation and Pain Following Cataract Surgery.” Clinical Ophthalmology (Auckland, N.Z.) 4 (September): 983–91.
  28. Pleyer, Uwe, Paul G. Ursell, and Paolo Rama. 2013. “Intraocular Pressure Effects of Common Topical Steroids for Post-Cataract Inflammation: Are They All the Same?” Ophthalmology and Therapy 2 (2): 55–72.
  29. Saad El Saman, Islam, Engy Mohamed Mostafa, Ahmed Gad Kamel, and Osama Ali Mohammed. 2018. “Comparison of Difluprednate 0.05% versus Prednisolone Acetate 1% Eye Drops Following Uneventful Cataract Surgery.” Journal of Clinical Ophthalmology 03 (01).
  30. Lane, Stephen S., and Edward J. Holland. 2013. “Loteprednol Etabonate 0.5% versus Prednisolone Acetate 1.0% for the Treatment of Inflammation after Cataract Surgery.” Journal of Cataract and Refractive Surgery 39 (2): 168–73.
  31. Herschler J. Increased intraocular pressure induced by repository corticosteroids. Am J Ophthalmol. 1976;82(1):90-93.
  32. 32.0 32.1 Yamamoto, Yumiko, Tsutomu Komatsu, Yuji Koura, Koji Nishino, Atsuki Fukushima, and Hisayuki Ueno. 2008. “Intraocular Pressure Elevation after Intravitreal or Posterior Sub-Tenon Triamcinolone Acetonide Injection.” Canadian Journal of Ophthalmology. Journal Canadien d’ophtalmologie 43 (1): 42–47.
  33. Kalina, R. E. 1969. “Increased Intraocular Pressure Following Subconjunctival Corticosteroid Administration.” Archives of Ophthalmology 81 (6): 788–90.
  34. Hayashi, Ken, and Hideyuki Hayashi. 2005. “Intravitreal versus Retrobulbar Injections of Triamcinolone for Macular Edema Associated with Branch Retinal Vein Occlusion.” American Journal of Ophthalmology 139 (6): 972–82.
  35. 35.0 35.1 Goñi, Francisco J., Ingeborg Stalmans, Philippe Denis, Jean-Philippe Nordmann, Simon Taylor, Michael Diestelhorst, Antonio R. Figueiredo, and David F. Garway-Heath. 2016. “Elevated Intraocular Pressure after Intravitreal Steroid Injection in Diabetic Macular Edema: Monitoring and Management.” Ophthalmology and Therapy 5 (1): 47–61.
  36. 36.0 36.1 Jones R III, Rhee DJ. Corticosteroid-induced ocular hypertension and glaucoma: a brief review and update of the literature. Curr Opin Ophthalmol. 2006;17(2):163-167.
  37. 37.0 37.1 Vedantham V. Intraocular pressure rise after intravitreal triamcinolone. Am J Ophthalmol. 2005;139(3):575.
  38. 38.0 38.1 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(2):573-576.
  39. Kiddee, Weerawat, Graham E. Trope, Lisa Sheng, Laura Beltran-Agullo, Michael Smith, M. Hermina Strungaru, Jasrajbir Baath, and Yvonne M. Buys. 2013. “Intraocular Pressure Monitoring Post Intravitreal Steroids: A Systematic Review.” Survey of Ophthalmology 58 (4): 291–310.
  40. Boyer, David S., Young Hee Yoon, Rubens Belfort Jr, Francesco Bandello, Raj K. Maturi, Albert J. Augustin, Xiao-Yan Li, et al. 2014. “Three-Year, Randomized, Sham-Controlled Trial of Dexamethasone Intravitreal Implant in Patients with Diabetic Macular Edema.” Ophthalmology 121 (10): 1904–14.
  41. Jaffe, Glenn J., Daniel Martin, David Callanan, P. Andrew Pearson, Brian Levy, Timothy Comstock, and Fluocinolone Acetonide Uveitis Study Group. 2006. “Fluocinolone Acetonide Implant (Retisert) for Noninfectious Posterior Uveitis: Thirty-Four-Week Results of a Multicenter Randomized Clinical Study.” Ophthalmology 113 (6): 1020–27.
  42. Campochiaro, Peter A., David M. Brown, Andrew Pearson, Sanford Chen, David Boyer, Jose Ruiz-Moreno, Bruce Garretson, et al. 2012. “Sustained Delivery Fluocinolone Acetonide Vitreous Inserts Provide Benefit for at Least 3 Years in Patients with Diabetic Macular Edema.” Ophthalmology 119 (10): 2125–32.
  43. Garrott, Helen M., and Mark J. Walland. 2004. “Glaucoma from Topical Corticosteroids to the Eyelids.” Clinical & Experimental Ophthalmology 32 (2): 224–26.
  44. Schwartzenberg GW, Buys YM. Glaucoma secondary to topical use of steroid cream. Can J Ophthalmol. 1999;34(4):222-225.
  45. 45.0 45.1 Opatowsky I, Feldman RM, Gross R, et al. Intraocular pressure elevation associated with inhalation and nasal corticosteroids. Ophthalmology.1995;102(2):177-179.
  46. Godel V, Feiler-Ofry V, Stein R. Systemic steroids and ocular fluid dynamics. I. Analysis of the sample as a whole: influence of dosage and duration of therapy. Acta Ophthalmol (Copenh). 1972;50(5):655-663
  47. Godel V, Feiler-Ofry V, Stein R. Sysemic steroids and ocular fluid dynamics. II. Systemic versus topical steroids. Acta Ophthalmol (Copenh).1972;50(5):664-676.
  48. Ticho, U., A. Durst, A. Licht, and S. Berkowitz. 1977. “Steroid-Induced Glaucoma and Cataract in Renal Transplant Recipients.” Israel Journal of Medical Sciences 13 (9): 871–74.
  49. Hovland, K. R., and P. P. Ellis. 1967. “Ocular Changes in Renal Transplant Patients.” American Journal of Ophthalmology 63 (2): 283–89.
  50. Tripathi, Ramesh C., Barbara S. Kirschner, Michael Kipp, Brenda J. Tripathi, David Slotwiner, Navaneet S. C. Borisuth, Theodore Karrison, and J. Terry Ernest. 1992. “Corticosteroid Treatment for Inflammatory Bowel Disease in Pediatric Patients Increases Intraocular Pressure.” Gastroenterology 102 (6): 1957–61.
  51. Garbe, E., J. LeLorier, J. F. Boivin, and S. Suissa. 1997. “Risk of Ocular Hypertension or Open-Angle Glaucoma in Elderly Patients on Oral Glucocorticoids.” Lancet 350 (9083): 979–82.
  52. Taliaferro, Kevin, Alexander Crawford, Justin Jabara, Jonathan Lynch, Edward Jung, Raimonds Zvirbulis, and Trevor Banka. 2018. “Intraocular Pressure Increases after Intraarticular Knee Injection with Triamcinolone but Not Hyaluronic Acid.” Clinical Orthopaedics and Related Research 476 (7): 1420–25.
  53. Dibildox, J. 2001. “Safety and Efficacy of Mometasone Furoate Aqueous Nasal Spray in Children with Allergic Rhinitis: Results of Recent Clinical Trials.” The Journal of Allergy and Clinical Immunology 108 (1 Suppl): S54-8.
  54. Seiberling, Kristin A., Dennis F. Chang, Janice Nyirady, Francine Park, and Christopher A. Church. 2013. “Effect of Intranasal Budesonide Irrigations on Intraocular Pressure.” International Forum of Allergy & Rhinology 3 (9): 704–7.
  55. Bui, Christina M., Heidi Chen, Yu Shyr, and Karen M. Joos. 2005. “Discontinuing Nasal Steroids Might Lower Intraocular Pressure in Glaucoma.” The Journal of Allergy and Clinical Immunology 116 (5): 1042–47.
  56. Mitchell, P., R. G. Cumming, and D. A. Mackey. 1999. “Inhaled Corticosteroids, Family History, and Risk of Glaucoma.” Ophthalmology 106 (12): 2301–6.
  57. Sihota, R., V. L. Konkal, T. Dada, H. C. Agarwal, and R. Singh. 2008. “Prospective, Long-Term Evaluation of Steroid-Induced Glaucoma.” Eye 22 (1): 26–30.
  58. Ferry AP, Harris WP, Nelson MH. Histopathologic features of subconjunctivally injected corticosteroids. Am J Ophthalmol. 1987;103(5):716-718.
  59. Tokuda Naoto, Inoue Jun, Yamazaki Izumi, Matsuzawa Akiko, Munemasa Yasunari, Kitaoka Yasushi, Takagi Hitoshi, and Ueno Satoki. 2012. “Effects of selective laser trabeculoplasty treatment in steroid-induced glaucoma.” Nippon Ganka Gakkai zasshi 116 (8): 751–57.
  60. Rubin, Benjamin, Anthony Taglienti, Robert F. Rothman, Craig H. Marcus, and Janet B. Serle. 2008. “The Effect of Selective Laser Trabeculoplasty on Intraocular Pressure in Patients with Intravitreal Steroid-Induced Elevated Intraocular Pressure.” Journal of Glaucoma 17 (4): 287–92.
  61. Choi, Eun Young, and David S. Walton. 2015. “Goniotomy for Steroid-Induced Glaucoma: Clinical and Tonographic Evidence to Support Therapeutic Goniotomy.” Journal of Pediatric Ophthalmology and Strabismus 52 (3): 183–88.
  62. Brusini, Paolo, Claudia Tosoni, and Marco Zeppieri. 2018. “Canaloplasty in Corticosteroid-Induced Glaucoma. Preliminary Results.” Journal of Clinical Medicine 7 (2).