Steroid-related Ocular Hypertension and Glaucoma


Elevation of IOP has been associated with both ocular and systemic administration of steroids (e.g. topical application to the eye or eyelids, sub-Tenon’s injection, intra-vitreal injection [or implant], steroid by mouth). Three quarters of all cases relate to the topical application of steroids to the eye.

If the elevated IOP is of sufficient magnitude and duration, damage to the optic nerve can occur with resulting visual field loss (steroid glaucoma)

The mechanism of elevated intraocular pressure is increased aqueous outflow resistance owing to morphological changes in the trabecular meshwork

With regard to this ‘steroid response’ the normal population can be divided into three groups:

  • high responders (5%): marked elevation of IOP by >15mmHg
  • moderate responders (30%): moderate elevation by 6-15mmHg
  • non-responders (65%): an elevation of up to 5mmHg is considered irrelevant in this instance

The higher the steroid potency, the greater the ocular hypertensive response. The ophthalmic steroids dexamethasone and prednisolone acetate are more likely to result in clinically significant increases in IOP when compared to fluorometholone and loteprednol.

Depot injections of steroid increase the risk of a significantly raised IOP in responders, with intravitreal steroids being a greater risk than subconjunctival or sub-tenon’s delivery

Predisposing factors

Chronic open angle glaucoma (COAG)
First degree relative with COAG
Childhood, especially below the age of 10 years

  • a small case series found that approx. 50% of children treated with high-dose systemic glucocorticoids developed an ocular hypertensive response

High myopia
Prescription of post-operative topical steroid
Self-administration where topical steroid preparations are available without prescription

Symptoms of glaucoma (steroid)

None in the early stages; visual loss later

Signs of glaucoma (steroid)

Raised intraocular pressure following use of topical steroid
If optic neuropathy is present, the condition clinically resembles COAG (although higher IOP compared to COAG, resulting in more rapid visual field and optic disc changes)
Can occur at any time (within weeks with potent drugs and after several months with weaker agents); onset rare with less than 3 weeks’ exposure

Differential diagnosis

Ocular hypertension
Secondary glaucoma (pigment dispersion, pseudo-exfoliation, neovascular, inflammatory [e.g. Posner-Schlossman syndrome or following anterior uveitis])

Management by optometrist

Practitioners should work within their scope of practice, and where necessary seek further advice or refer the patient elsewhere

GRADE* Level of evidence and strength of recommendation always relates to the statement(s) immediately above

Non pharmacological

A baseline measurement of IOP should always be taken prior to commencement of steroid therapy. Patients newly begun on ocular steroid therapy should have their IOPs measured again after 2 weeks, then every 4 weeks for 2-3 months, then 6-monthly if therapy is to continue

It has been recommended in patients receiving intravitreal steroids (injections or implants) to measure IOP at 30 minutes, at 1 week, 2 weeks and then monthly for up to 6 months

If a steroid response is detected, discuss with the prescribing clinician the possibility of discontinuing steroid therapy (the chronic steroid response usually resolves in 1-4 weeks, whilst the acute response may resolve within a few days of cessation of steroid therapy). The IOP usually returns to normal within 2-4 weeks after discontinuation, but if the steroid therapy has continued for 18 months or more, the raised IOP may persist for longer


Patient may need topical anti-glaucoma medication (discuss with prescribing clinician)
(GRADE*: Level of evidence=low, Strength of recommendation=strong)

Management category

If high steroid responder, elevated IOP due to intravitreal steroids or presence of optic neuropathy

A3: possible first aid measures followed by urgent referral to an ophthalmologist (within one week)

If the optometrist is the prescribing clinician, may need to discontinue steroid or switch to ‘non-penetrating’ steroid and monitor IOP until it reaches an acceptable level. Patient may need short-term ocular hypotensive medication. In this situation, referral may not be necessary

B3: management to resolution

Possible management in secondary care or local primary/community pathways where available

Additional guidance may be available

Alternative therapy with topical steroids that are less likely to cause raised intra-ocular pressure and/or with NSAIDs
Anti-glaucoma management (medical ± surgical including laser)

Evidence base

*GRADE: Grading of Recommendations Assessment, Development and Evaluation (

Sources of evidence

Ahmadi N, Snidvongs K, Kalish L, Sacks R, Tumuluri K, Wilcsek G, Harvey R. Intranasal corticosteroids do not affect intraocular pressure or lens opacity: a systematic review of controlled trials. Rhinology. 2015;53(4):290-302

Dibas A, Yorio T Glucocorticoid therapy and ocular hypertension. Eur J Pharmacol. 2016;787:57-71

Jones R, Rhee DJ. Corticosteroid-induced ocular hypertension and glaucoma: a brief review and update of the literature. Curr Opin Ophthalmol 2006;17:163-7

Kersey JP, Broadway DC. Corticosteroid-induced glaucoma: a review of the literature. Eye 2006;20:407-16

Kiddee W, Trope GE, Sheng L, Beltran-Agullo L, Smith M, Strungaru MH, Baath J, Buys YM. Intraocular pressure monitoring post intravitreal steroids: a systematic review. Surv Ophthalmol. 2013;58:291-310

Mazzarella S, Mateo C, Freixes S, Burés-Jelstrup A, Rios J, Navarro R, García-Arumí J, Corcóstegui B, Arrondo E. Effect of intravitreal injection of dexamethasone 0.7 mg (Ozurdex®) on intraocular pressure in patients with macular edema. Ophthalmic Res. 2015;54(3):143-9

Phulke S, Kaushik S, Kaur S, Pandav SS. Steroid-induced glaucoma: an avoidable irreversible blindness. J Curr Glaucoma Pract. 2017;11(2):67-72

Pleyer U, Ursell PG, Rama P. Intraocular pressure effects of common topical steroids for post-cataract inflammation: are they all the same? Ophthalmol Ther. 2013;2:55-72

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. pii: S0039-6257(20)30024-2


What is Steroid-related Ocular Hypertension and Glaucoma?

When some patients are treated with steroids (as eye drops, tablets, injections, implants) it can cause the pressure inside their eye to rise. 35% of the population are at risk of developing this problem. As the raised pressure does not usually cause symptoms, the patient may be unaware that the eye pressure is rising and if not identified can lead to glaucoma. Glaucoma is a disease in which raised eye pressure can damage the nerve fibres of the retina (the light-sensitive layer at the back of the eye) and cause selective but irreparable loss of the eye’s field of vision.

How is Steroid-related Ocular Hypertension and Glaucoma managed?

Stopping the steroid that causes the condition, if this is appropriate, usually allows the eye pressure to return to normal. If this does not happen, the condition may have to be treated as if it were an ordinary case of glaucoma (of the type known as ‘open angle’), using eye drops or possibly laser treatment or surgery.

Glaucoma (steroid)
Version 13
Date of search 21.02.22
Date of revision 05.09.22
Date of publication 20.12.22
Date for review 20.02.24
© College of Optometrists 

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