Continuing Education Activity

Steroids are one of the most commonly prescribed drugs, used mainly to treat various autoimmune and inflammatory conditions. Although they have numerous benefits, steroid usage can also cause many adverse effects. Some of these effects are on the eye, the most important being steroid-induced glaucoma and cataracts. Ocular hypertension can also occur after intranasal, inhalational, systemic use, and dermatological applications. Several factors seem to play a crucial role in causing elevated intraocular pressure (IOP), mostly due to the increase of the resistance in the outflow mechanisms of the trabecular meshwork (TM). This activity describes steroid-induced glaucoma and its pathophysiology and highlights the role of the interprofessional team in its prevention and treatment.

Objectives:

• Describe the epidemiology of steroid-induced glaucoma.
• Review the presentation of a patient with steroid-induced glaucoma.
• Summarize the treatment options for steroid-induced glaucoma.
• Outline the importance of improving care coordination among interprofessional team members to improve outcomes for patients affected by steroid-induced glaucoma.

Introduction

Steroids are one of the most commonly prescribed drugs, used mainly to treat various autoimmune and inflammatory conditions. Although it has numerous benefits, steroid usage can cause many adverse effects on the eye, the most important being steroid-induced glaucoma and cataract.[1][2] Steroid-induced iatrogenic glaucoma was described for the first time in the 1950s, with the observation of glaucoma following the use of systemic adrenocorticotropic hormones and topical or systemic steroids.[3] 

Several factors seem to play a crucial role in causing elevated intraocular pressure (IOP), mostly due to the increase of the resistance in the outflow mechanisms of the trabecular meshwork (TM). It has been shown that glucocorticoids (GC) can alter the microstructure by inducing cross-links in the network of the actin fiber.[4] There also appears to be an increase in collagen and fibronectin deposits in the juxtacanalicular region's extracellular matrix.[5] Corticosteroids have also been shown to influence the turnover of substances and enzymes (i.e., stromelysin, metalloproteinases, tissue plasminogen activator, etc.) in the TM, which give rise to increased outflow resistance in this important structure that regulates IOP levels.[6]

Etiology

Ocular hypertension (OHT) can occur after steroid use in susceptible individuals. Steroid-induced glaucoma (SIG), a form of secondary glaucoma, can occur when elevated intraocular pressure (IOP) gives rise to irreversible optic neuropathy. The term "steroid responder" (SR) is used to indicate individuals that show elevated IOP after steroid use, which has been defined in current literature as IOP above 21 mmHg to 24 mmHg and/or an increase of greater than 5 to 10 mmHg compared to baseline with clinical significance.[7]

IOP elevations are seen most commonly after topical, periocular, or intraocular administration in steroid responders. OHT can also occur after intranasal, inhalational, systemic use, and dermatological applications.[8] Intraocular pressure (IOP) increase usually occurs 3 to 6 weeks following topical steroid use. However, it may occur earlier. IOP tends to return to normal values about two weeks after cessation of steroid eyedrops. Corticosteroid eye injections, however, can give rise to an acute rise in IOP.[9] Other routes of GC may affect IOP; however, they tend to be less clinically significant when compared to ocular routes.

Epidemiology

The exact prevalence of SR is not known; however, studies have shown that more than 30% of individuals show a moderate rise of IOP (6 to 15 mmHg) after topical cortisone use, while about 5% are highly responsive (IOP elevations >16 mmHg).[10]  Several studies have reported the incidence in the pediatric population to be similar, if not more frequent, compared to adults.[11] Acute elevated IOP levels in SR individuals with primary-open angle glaucoma (POAG) and other forms of glaucoma can worsen existing glaucomatous optic neuropathy.  

Based on the IOP response to the topical administration of betamethasone and dexamethasone, Armaly and Becker[10] suggested three categories:

1. High responders (4 to 6% of the population): developed an IOP greater than 31 mmHg or a rise of more than 15 mmHg from baseline.
2. Moderate responders (about 1/3 of the population): developed an IOP between 25 to 31 mmHg or a rise of 6 to 15 mmHg from baseline.
3. Non-responders (about 2/3 of the population): most individuals had an IOP of less than 20 mmHg or a rise of less than 6 mmHg from baseline.

Studies have shown that there are numerous risk factors for the development of high responsiveness, which include: diagnosis or family history of primary open-angle glaucoma (possibly due to the different expression of steroid receptors and isoforms in the TM), diabetes mellitus, high myopia, and, connective tissue disorders such as rheumatoid arthritis.[12][13][14][15][16] The elderly population tends to be more susceptible, as are children less than six years of age.[17][18] Studies have shown the odds ratio of developing SG in older patients to be as high as 1.72 after using topical cortisone eye drops.[19]

Pathophysiology

SIG is considered a type of secondary open-angle glaucoma caused by increased resistance to the aqueous outflow at the TM level. In this condition, there is increased production and decreased destruction of the extracellular matrix of the TM.[20] There is increased deposition of glycosaminoglycans, fibronectin, elastin, and type IV collagen and reduced activity of matrix metalloproteinases. TM cells have glucocorticoid receptors, and steroids may act on them to alter cell migration and phagocytosis.[21] This reaction causes decreased cellularity of the TM and increased extracellular matrix deposition, thus increasing aqueous outflow resistance and a rise in IOP. Glaucoma may develop if the IOP elevation is of sufficient magnitude and duration, thus leading to progressive damage to the optic nerve and visual field.

Cortisone Treatment Route

The route of administration is also very important in the effects of IOP elevations. Cortisone therapy can be administered topically on the ocular surface, periocular, intraocular, orally, intravenously, nasally, inhaled, transcutaneous, and via endogenous production. The most common forms of SIG are caused by topical routes, representing about 75% of cases.[7]

Topical cortisones are often used for conjunctivitis, allergies, ocular inflammations, and treatment regimens after laser and surgery procedures.[22] Drops can be dispensed without a prescription in most countries; thus, self-administered therapy can explain the high incidence of SID in both children and adults. Elevations in IOP elevation, which can range from 6 to 22 mmHg and last up to months after therapy, tend to be more common with forms of cortisone, such as prednisolone, dexamethasone, clobetasone, betamethasone, and fluorometholone.[23] Newer topical formulations, such as etabonate, loteprednol, rimexolone, or difluprednate that have less influence on IOP tend to be preferred when possible. Elevations in IOP can last up to 18 months after cessation of topical therapy.[24][25]

The intraocular routes, in which GC is administered using intravitreal injections or by sustained-released intravitreal implants, have grown considerably in the past decade to treat choroidal, macular, and retinal diseases.[26] GC therapy is usually administered with triamcinolone acetonide, fluocinolone acetonide, and dexamethasone. OHT and SIG are more commonly seen with fluocinolone acetonide, while dexamethasone tends to have lower risks among the intravitreal options.[27] Sustained-release implants with fluocinolone acetonide (non-biodegradable) and dexamethasone (biodegradable) can be advantageous for individuals requiring numerous intravitreal cortisone treatments. Fluocinolone acetonide has been shown to have a greater risk of OHT and SID when compared to dexamethasone, with an incidence ranging from 11 to 37% and up to 79 % in patients with uveitis.[28] Increases in IOP tend to be seen within a few weeks, with maximum levels reached after 28 weeks, while decreases in IOP after 9 to 12 months.[29]

Studies have shown that about 75% of patients with fluocinolone acetonide implants required IOP lowering medication, and one-third required glaucoma surgery.[28] In comparison, patients with dexamethasone implants with OHT and SID were reported to be much less, with 26.5% and up to 3.2% requiring local drops and surgery, respectively.[30]

The periocular routes involve injection within various spaces, which include the sub-Tenon, subconjunctival, orbital floor, or retrobulbar spaces. The sub-Tenon option is the periocular route most used in a clinical setting and represents a higher risk of OHT and SID in responders, possibly due to the closeness to the anterior chamber angle.[31] In a multicenter study based on individuals treated with different types of periocular cortisone treatments for uveitis, the incidence of elevated IOP greater than 24 mmHg was about 35%, with 2.4% needing glaucoma surgery.[32]

Systemic GC is typically prescribed for a variety of chronic inflammatory diseases. The systemic route comprises oral ingestion, local application of creams and ointments, intravenous therapy, nasal spray, and pulmonary inhalation. The risk of OHT and SIG with systemic therapy tends to be less than via ocular routes; however, clinically important IOP elevations can be seen for months and years in individuals treated with long-term systemic cortisone.[33] Studies have shown that about 20% of patients with glaucoma were on systemic cortisone treatments. These individuals tended to have more severe functional damage in visual fields.[34]

The odds ratio of developing elevated IOP after chronic system cortisone use has been reported to range from 1.4 to 1.9 based on doses administered, with a mean increase of 1.4 mmHg for each 10 mg increase in the daily dose of cortisone.[19][35] A thorough metanalysis based on the effects of IOP with systemic cortisone concluded that chronic oral steroid users are at risk of elevated IOP, especially those with existing glaucoma, and that inhaled and intranasal routes have fewer chances of developing OHT if cortisone doses are not extremely high.[8]

The excess production of endogenous cortisone due to endocrine disorders rarely causes SIG.[18]

History and Physical

Any form of steroid administration can cause glaucoma. It may occur after the administration of topical steroids for a relatively trivial condition, after the postoperative administration of steroids for refractive surgeries, or after prolonged systemic corticosteroid treatment for inflammatory conditions.[33] Similar to other forms of glaucoma, SIG is often asymptomatic and detected incidentally by an ophthalmologist.[36] In severe cases, patients may complain of blurred vision or notice a visual field defect. Blurred vision may be due to corneal edema or steroid-induced posterior subcapsular cataract. An acute rise in IOP may sometimes cause a brow or eye ache.

On examination, the eye is usually unremarkable. The IOP becomes elevated beyond the normal range of 10 mmHg to 22 mmHg, and upon soliciting a history of steroid use, the patient is said to have steroid-induced hypertension. As for all types of glaucoma, tonometry is crucial in diagnosing SIG.[37] Prolonged IOP rise may cause progression to steroid-induced glaucoma, with signs of glaucomatous optic neuropathy and the characteristic glaucomatous visual field defects.

The age of the patient may influence the clinical picture of SIG. Children may present with enlarged corneal diameters and buphthalmos similar to congenital glaucoma. Elderly patients who have received steroid treatment and had it subsequently discontinued may present as normal-tension glaucoma. It is critical to ask about a history of steroid use when presented with a patient with elevated IOP.

Evaluation

The patient's history may give a clue to the underlying etiology of this condition. Patients with vernal conjunctivitis or another allergic conjunctivitis may use steroid eye drops for a long time. Patients may be on topical steroid treatment for postsurgical conditions like PRK or may have an implanted depot steroid. Renal transplant patients are another group of likely candidates to develop this condition.

The evaluation of individuals with SID is similar to all forms of OHT and glaucoma. The assessment includes recording visual acuity, thorough anterior and posterior segment examination, measurement of IOP (tonometry), visual field testing, ocular coherence tomography (OCT) testing, and gonioscopy. Tonometry is fundamental in assessing OHT and SID, which ideally should be performed with the standard gold technique of Goldmann applanation tonometry (GAT).[38][39][40] Alternative tonometers like iCare, which is easier to perform and does not require anesthesia drops and fluorescein, can be considered when GAT proves to be difficult, such as in children, noncollaborative individuals, and the bedridden.[41]

Treatment / Management

The first step in the management of SIG is the discontinuation of steroids, if clinically possible.[42] Removal of repository steroids is also indicated. If it is difficult to discontinue steroids completely, the dose should be reduced, or a weaker steroid should be substituted. Antiglaucoma medications can be added to control the IOP.[43][44]

The three modalities of management of steroid-induced glaucoma are:

1. Medical management: medical management of this condition is similar to that of primary open-angle glaucoma. The agents which may be used include beta-blockers, prostaglandin analogs, alpha-2 agonists, and carbonic anhydrase inhibitors. Beta-blockers tend to be the first-line agents in this condition.[45] 
2. Laser trabeculoplasty: argon laser trabeculoplasty(ALT) and selective laser trabeculoplasty (SLT) may be considered if medical management is unsuccessful and there is a threat of impending optic nerve damage. It may also be considered in patients experiencing undesirable side effects with antiglaucoma drugs. The disadvantages of laser include that the IOP effect may last several months, and retreatment is usually required.
3. Surgical management: surgery is indicated in those patients who fail to respond to medical and laser therapies. It may also be indicated in those patients who may be expected to have further exposure to steroids. The most commonly employed surgical procedure is trabeculectomy; other options include deep sclerectomy, canaloplasty, tube shunt surgeries, or cyclophotocoagulation procedures.[46][47][48][49][50]

Differential Diagnosis

Elevated IOP can be caused by many things, even with concurrent steroid use. The steroid-induced rises in IOP are reversible on discontinuation. This differentiates it from glaucoma. Below is a list of differential diagnoses that can give rise to high levels of IOP:

• Primary open-angle glaucoma (POAG)
• Angle-closure glaucoma
• Angle-recession glaucoma
• Pigmentary glaucoma
• Plateau iris glaucoma
• Pseudoexfoliation glaucoma
• Uveitic glaucoma

Prognosis

Elevated IOP from steroid-induced glaucoma shares a similar prognosis to other types of glaucoma. If the IOP is controlled, the likelihood of glaucoma developing is very low.

Deterrence and Patient Education

Patients taking steroids should be educated on the risks of IOP elevation. While steroids will have a minimal effect on the IOP of most patients, there is a small population that will develop a significant increase in IOP. Providers should inform patients that already have glaucoma that the risk of IOP elevation and glaucoma progression with steroids is greater than in the general population.[33]

Pearls and Other Issues

Although steroid use is of utmost benefit in many autoimmune and inflammatory conditions, regular monitoring of the patient’s ocular condition is mandatory to detect this complication at the earliest stage. This workup should include baseline IOP measurements, followed by checking IOP after two weeks, then every 4 to 6 weeks for about three months, and then six-monthly (if the initial response is ruled out). Although steroid-induced glaucoma is a dangerous and potentially blinding condition, it is manageable by early detection and prompt initiation of anti-glaucoma treatment.

Enhancing Healthcare Team Outcomes

Steroids are widely prescribed by clinicians, including MDs, DOs, NPs, and PAs, as part of an interprofessional team that also includes nurses and pharmacists. One of the most dangerous side effects of these drugs is elevated IOP. Thus, it is essential for the entire interprofessional healthcare team to monitor the patient for eye symptoms and refer them to an ophthalmic clinician or optometrist for the screening of glaucoma.[3] If the steroid cannot be tapered, the patient may need to start on anti-glaucoma medications. When treating glaucoma, the prognosis is good.[51] Pharmacists can consult on the steroid dosing as well as the anti-glaucoma medications when needed. Nurses will serve as coordinators for the various clinicians on the case, offer patient counsel, and in some instances, administer medication. When treating glaucoma, the prognosis is good.[51] The interprofessional care model will yield the best patient outcomes with the fewest adverse events. [Level 5]

Review Questions

• Access free multiple choice questions on this topic.
• Comment on this article.

References

1.

Roberti G, Oddone F, Agnifili L, Katsanos A, Michelessi M, Mastropasqua L, Quaranta L, Riva I, Tanga L, Manni G. Steroid-induced glaucoma: Epidemiology, pathophysiology, and clinical management. Surv Ophthalmol. 2020 Jul-Aug;65(4):458-472. [PubMed: 32057761]

2.

Bojikian KD, Nobrega P, Roldan A, Forrest SL, Tsukikawa M, Chen PP. Incidence of and Risk Factors for Steroid Response After Cataract Surgery in Patients With and Without Glaucoma. J Glaucoma. 2021 Apr 01;30(4):e159-e163. [PubMed: 33428351]

3.

Phulke S, Kaushik S, Kaur S, Pandav SS. Steroid-induced Glaucoma: An Avoidable Irreversible Blindness. J Curr Glaucoma Pract. 2017 May-Aug;11(2):67-72. [PMC free article: PMC5577123] [PubMed: 28924342]

4.

Clark AF, Wilson K, McCartney MD, Miggans ST, Kunkle M, Howe W. Glucocorticoid-induced formation of cross-linked actin networks in cultured human trabecular meshwork cells. Invest Ophthalmol Vis Sci. 1994 Jan;35(1):281-94. [PubMed: 8300356]

5.

Yue BY. The extracellular matrix and its modulation in the trabecular meshwork. Surv Ophthalmol. 1996 Mar-Apr;40(5):379-90. [PubMed: 8779084]

6.

Jones R, Rhee DJ. Corticosteroid-induced ocular hypertension and glaucoma: a brief review and update of the literature. Curr Opin Ophthalmol. 2006 Apr;17(2):163-7. [PubMed: 16552251]

7.

Sheppard JD, Comstock TL, Cavet ME. Impact of the Topical Ophthalmic Corticosteroid Loteprednol Etabonate on Intraocular Pressure. Adv Ther. 2016 Apr;33(4):532-52. [PMC free article: PMC4846687] [PubMed: 26984315]

8.

Wijnants D, Stalmans I, Vandewalle E. The Effects of Intranasal, Inhaled and Systemic Glucocorticoids on Intraocular Pressure: A Literature Review. J Clin Med. 2022 Apr 03;11(7) [PMC free article: PMC8999749] [PubMed: 35407615]

9.

Lebrize S, Arnould L, Bourredjem A, Busch C, Rehak M, Massin P, Barbosa-Breda J, Lupidi M, Mariotti C, Hamza M, Grise-Dulac A, Gabrielle PH, Baillif S, Creuzot-Garcher C. Intraocular Pressure Changes After Intravitreal Fluocinolone Acetonide Implant: Results from Four European Countries. Ophthalmol Ther. 2022 Jun;11(3):1217-1229. [PMC free article: PMC9114211] [PubMed: 35426623]

10.

Armaly MF, Becker B. Intraocular pressure response to topical corticosteroids. Fed Proc. 1965 Nov-Dec;24(6):1274-8. [PubMed: 5853148]

11.

Kwok AK, Lam DS, Ng JS, Fan DS, Chew SJ, Tso MO. Ocular-hypertensive response to topical steroids in children. Ophthalmology. 1997 Dec;104(12):2112-6. [PubMed: 9400772]

12.

Patel GC, Liu Y, Millar JC, Clark AF. Glucocorticoid receptor GRβ regulates glucocorticoid-induced ocular hypertension in mice. Sci Rep. 2018 Jan 16;8(1):862. [PMC free article: PMC5770444] [PubMed: 29339763]

13.

Bartlett JD, Woolley TW, Adams CM. Identification of high intraocular pressure responders to topical ophthalmic corticosteroids. J Ocul Pharmacol. 1993 Spring;9(1):35-45. [PubMed: 8463731]

14.

Becker B, Bresnick G, Chevrette L, Kolker AE, Oaks MC, Cibis A. Intraocular pressure and its response to topical corticosteroids in diabetes. Arch Ophthalmol. 1966 Oct;76(4):477-83. [PubMed: 5928134]

15.

Podos SM, Becker B, Morton WR. High myopia and primary open-angle glaucoma. Am J Ophthalmol. 1966 Dec;62(6):1038-43. [PubMed: 5957877]

16.

Hoffmeister RT. Methotrexate therapy in rheumatoid arthritis: 15 years experience. Am J Med. 1983 Dec 30;75(6A):69-73. [PubMed: 6660241]

17.

Gupta S, Shah P, Grewal S, Chaurasia AK, Gupta V. Steroid-induced glaucoma and childhood blindness. Br J Ophthalmol. 2015 Nov;99(11):1454-6. [PubMed: 26002945]

18.

Marcus MW, Müskens RP, Ramdas WD, Wolfs RC, De Jong PT, Vingerling JR, Hofman A, Stricker BH, Jansonius NM. Corticosteroids and open-angle glaucoma in the elderly: a population-based cohort study. Drugs Aging. 2012 Dec;29(12):963-70. [PubMed: 23150239]

19.

Garbe E, LeLorier J, Boivin JF, Suissa S. Risk of ocular hypertension or open-angle glaucoma in elderly patients on oral glucocorticoids. Lancet. 1997 Oct 04;350(9083):979-82. [PubMed: 9329512]

20.

Wei M, Chen LM, Huang ZY, Zhang GW, Guan HJ, Ji M. Expression profile analysis to identify potential gene changes induced by dexamethasone in the trabecular meshwork. Int J Ophthalmol. 2022;15(8):1240-1248. [PMC free article: PMC9358186] [PubMed: 36017046]

21.

Mohd Nasir NA, Agarwal R, Krasilnikova A, Sheikh Abdul Kadir SH, Iezhitsa I. Effect of dexamethasone on the expression of MMPs, adenosine A1 receptors and NFKB by human trabecular meshwork cells. J Basic Clin Physiol Pharmacol. 2020 Jul 22;31(6) [PubMed: 32697755]

22.

Campochiaro PA, Han YS, Mir TA, Kherani S, Hafiz G, Krispel C, Liu TYA, Wang J, Scott AW, Zimmer-Galler I. Increased Frequency of Topical Steroids Provides Benefit in Patients With Recalcitrant Postsurgical Macular Edema. Am J Ophthalmol. 2017 Jun;178:163-175. [PubMed: 28392176]

23.

Abadia B, Calvo P, Ferreras A, Bartol F, Verdes G, Pablo L. Clinical Applications of Dexamethasone for Aged Eyes. Drugs Aging. 2016 Sep;33(9):639-46. [PubMed: 27566619]

24.

Shokoohi-Rad S, Daneshvar R, Jafarian-Shahri M, Rajaee P. Comparison between Betamethasone, Fluorometholone and Loteprednol Etabonate on intraocular pressure in patients after keratorefractive surgery. J Curr Ophthalmol. 2018 Jun;30(2):130-135. [PMC free article: PMC6033780] [PubMed: 29988925]

25.

Sng CC, Ang M, Barton K. Uveitis and glaucoma: new insights in the pathogenesis and treatment. Prog Brain Res. 2015;221:243-69. [PubMed: 26518082]

26.

Amoaku WM, Ghanchi F, Bailey C, Banerjee S, Banerjee S, Downey L, Gale R, Hamilton R, Khunti K, Posner E, Quhill F, Robinson S, Setty R, Sim D, Varma D, Mehta H. Diabetic retinopathy and diabetic macular oedema pathways and management: UK Consensus Working Group. Eye (Lond). 2020 Jun;34(Suppl 1):1-51. [PMC free article: PMC7337227] [PubMed: 32504038]

27.

Aref AA, Scott IU, Oden NL, Ip MS, Blodi BA, VanVeldhuisen PC., SCORE Study Investigator Group. Incidence, Risk Factors, and Timing of Elevated Intraocular Pressure After Intravitreal Triamcinolone Acetonide Injection for Macular Edema Secondary to Retinal Vein Occlusion: SCORE Study Report 15. JAMA Ophthalmol. 2015 Sep;133(9):1022-9. [PMC free article: PMC6639714] [PubMed: 26086920]

28.

Bollinger KE, Smith SD. Prevalence and management of elevated intraocular pressure after placement of an intravitreal sustained-release steroid implant. Curr Opin Ophthalmol. 2009 Mar;20(2):99-103. [PubMed: 19248312]

29.

Parrish RK, Traverso CE, Green K, Danis RP., FAME Study Group. Quantitative Assessment of Optic Nerve Changes in Patients With Diabetic Macular Edema Treated With Fluocinolone Acetonide Vitreous Implants. Ophthalmic Surg Lasers Imaging Retina. 2016 May 01;47(5):418-25. [PubMed: 27183545]

30.

Rajesh B, Zarranz-Ventura J, Fung AT, Busch C, Sahoo NK, Rodriguez-Valdes PJ, Sarao V, Mishra SK, Saatci AO, Udaondo Mirete P, Querques G, Farah ME, Lanzetta P, Arevalo JF, Kodjikian L, Chhablani J., for International Ozurdex Study Group. Safety of 6000 intravitreal dexamethasone implants. Br J Ophthalmol. 2020 Jan;104(1):39-46. [PubMed: 31040132]

31.

McGhee CN, Dean S, Danesh-Meyer H. Locally administered ocular corticosteroids: benefits and risks. Drug Saf. 2002;25(1):33-55. [PubMed: 11820911]

32.

Sen HN, Vitale S, Gangaputra SS, Nussenblatt RB, Liesegang TL, Levy-Clarke GA, Rosenbaum JT, Suhler EB, Thorne JE, Foster CS, Jabs DA, Kempen JH. Periocular corticosteroid injections in uveitis: effects and complications. Ophthalmology. 2014 Nov;121(11):2275-86. [PMC free article: PMC4254355] [PubMed: 25017415]

33.

Razeghinejad MR, Katz LJ. Steroid-induced iatrogenic glaucoma. Ophthalmic Res. 2012;47(2):66-80. [PubMed: 21757964]

34.

Bower T, Samek DA, Mohammed A, Mohammed A, Kasner P, Camoriano D, Kasner O. Systemic medication usage in glaucoma patients. Can J Ophthalmol. 2018 Jun;53(3):242-245. [PubMed: 29784160]

35.

Tripathi RC, Kirschner BS, Kipp M, Tripathi BJ, Slotwiner D, Borisuth NS, Karrison T, Ernest JT. Corticosteroid treatment for inflammatory bowel disease in pediatric patients increases intraocular pressure. Gastroenterology. 1992 Jun;102(6):1957-61. [PubMed: 1587414]

36.

Brusini P, Salvetat ML, Zeppieri M. It Is All about Pressure. J Clin Med. 2022 Jun 23;11(13) [PMC free article: PMC9267730] [PubMed: 35806926]

37.

Brusini P, Salvetat ML, Zeppieri M. How to Measure Intraocular Pressure: An Updated Review of Various Tonometers. J Clin Med. 2021 Aug 27;10(17) [PMC free article: PMC8456330] [PubMed: 34501306]

38.

Bader J, Zeppieri M, Havens SJ. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Dec 12, 2023. Tonometry. [PubMed: 29630277]

39.

Salvetat ML, Zeppieri M, Tosoni C, Brusini P., Medscape. Baseline factors predicting the risk of conversion from ocular hypertension to primary open-angle glaucoma during a 10-year follow-up. Eye (Lond). 2016 Jun;30(6):784-95. [PMC free article: PMC4906466] [PubMed: 27174381]

40.

Zeppieri M, Gurnani B. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jun 11, 2023. Applanation Tonometry. [PubMed: 35881737]

41.

Brusini P, Salvetat ML, Zeppieri M, Tosoni C, Parisi L. Comparison of ICare tonometer with Goldmann applanation tonometer in glaucoma patients. J Glaucoma. 2006 Jun;15(3):213-7. [PubMed: 16778643]

42.

Lam CS, Umi Kalthum MN, Norshamsiah MD, Bastion M. Case series of children with steroid-Induced glaucoma. Malays Fam Physician. 2018;13(3):32-37. [PMC free article: PMC6382086] [PubMed: 30800232]

43.

Shroff S, Thomas RK, D'Souza G, Nithyanandan S. The effect of inhaled steroids on the intraocular pressure. Digit J Ophthalmol. 2018;24(3):6-9. [PMC free article: PMC6380256] [PubMed: 30800006]

44.

Csorba A, Soproni A, Maneschg O, Nagy ZZ, Szamosi A. [Application of corticosteroid eye drops for allergic eye diseases in children]. Orv Hetil. 2019 Mar;160(9):329-337. [PubMed: 30798620]

45.

Badrinarayanan L, Rishi P, George R, Isaac N, Rishi E., Sankara Nethralaya Vitreo-Retinal group (SNVR). Incidence, Risk Factors, Treatment, and Outcome of Ocular Hypertension following Intravitreal Steroid Injections: A Comparative Study. Ophthalmologica. 2022;245(5):431-438. [PubMed: 35468616]

46.

Senthil S, Rao HL, Ali MH, Krishnamurthy R, Dikshit S, Choudhari N, Sastry R, Garudadri C. Long-term outcomes and risk factors for failure of glaucoma filtering surgery in eyes with vernal keratoconjunctivitis and steroid-induced glaucoma. Indian J Ophthalmol. 2022 Mar;70(3):820-825. [PMC free article: PMC9114571] [PubMed: 35225522]

47.

Elhofi A, Helaly HA. Outcome of Primary Nonpenetrating Deep Sclerectomy in Patients with Steroid-Induced Glaucoma. J Ophthalmol. 2018;2018:9215650. [PMC free article: PMC5904771] [PubMed: 29850218]

48.

Brusini P, Tosoni C, Zeppieri M. Canaloplasty in Corticosteroid-Induced Glaucoma. Preliminary Results. J Clin Med. 2018 Feb 11;7(2) [PMC free article: PMC5852447] [PubMed: 29439499]

49.

Gedde SJ, Feuer WJ, Lim KS, Barton K, Goyal S, Ahmed II, Brandt JD., Primary Tube Versus Trabeculectomy Study Group. Treatment Outcomes in the Primary Tube Versus Trabeculectomy Study after 5 Years of Follow-up. Ophthalmology. 2022 Dec;129(12):1344-1356. [PMC free article: PMC9691551] [PubMed: 35835337]

50.

Abdelmassih Y, Tomey K, Khoueir Z. Micropulse Transscleral Cyclophotocoagulation. J Curr Glaucoma Pract. 2021 Jan-Apr;15(1):1-7. [PMC free article: PMC8322594] [PubMed: 34393449]

51.

Nuyen B, Weinreb RN, Robbins SL. Steroid-induced glaucoma in the pediatric population. J AAPOS. 2017 Feb;21(1):1-6. [PubMed: 28087345]

Disclosure: Kaberi Feroze declares no relevant financial relationships with ineligible companies.

Disclosure: Marco Zeppieri declares no relevant financial relationships with ineligible companies.

Disclosure: Leila Khazaeni declares no relevant financial relationships with ineligible companies.