Glaucoma (steroid)

The CMGs are guidelines on the diagnosis and management of a range of common and rare, but important, eye conditions that present with varying frequency in primary and first contact care.

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Aetiology

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)
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 an accumulation of extracellular matrix material 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 >16mmHg
  • 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.

Predisposing factors

Primary open angle glaucoma (POAG)
First degree relative with POAG
Childhood
High myopia
Diabetes

Symptoms

None in the early stages; visual loss later

Signs

Raised intraocular pressure following use of topical steroid
If optic neuropathy is present, the condition clinically resembles POAG (although higher IOP compared to POAG, 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

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

Management by optometrist

Practitioners should recognise their limitations 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 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)

Pharmacological

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

Management category

A3: possible first aid measures followed by urgent referral to an ophthalmologist
If the optometrist is the prescribing clinician, 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 by ophthalmologist

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 (www.gradeworkinggroup.org)

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

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

Lay summary

The pressure inside the eye can rise if a patient is treated with steroids, either as eye drops, injection into the eye tissues, tablets or by injection. 35% of the population is at risk of developing this problem. If the raised pressure is not identified, glaucoma can result. This 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.

Stopping the steroid that causes the condition, if this is medically possible, 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 11
Date of search 20.12.17
Date of revision 22.02.18
Date of publication 09.05.18
Date for review 19.12.19
© College of Optometrists 

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