01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Corticosteroids can increase resistance to aqueous outflow in susceptible eyes. The resulting pressure rise may be discovered at a planned check before any symptoms or nerve damage occur. If the rise is missed or sustained, glaucomatous optic neuropathy can develop. The adverse response is related to the patient's susceptibility and the exposure, so one fixed interval or a reassuring previous course cannot guarantee safety during every future prescription.
The practical challenge is that the steroid may be treating a sight-threatening or systemic condition. Inflammation can itself elevate pressure, and controlling it remains essential. Management therefore requires a joined plan: establish the likely mechanism, assess current nerve risk, decide whether steroid exposure can be changed safely, and lower pressure when necessary. A dispensing or primary-care review should make sure that the intended ophthalmic monitoring is actually occurring, rather than either renewing indefinitely or withholding necessary treatment because a review letter is late.
Key points
- Steroid-induced ocular hypertension is raised pressure related to corticosteroid exposure; steroid-induced glaucoma additionally involves established optic nerve damage.
- Pressure elevation is often symptomless, so monitoring should be planned when treatment is started and revisited after dose or route changes.
- Ask about eye drops, ointments, periocular and intravitreal treatment, oral therapy and other steroid exposure rather than relying on the current eye-drop list alone.
- Consider pre-existing glaucoma, a previous steroid pressure response and the intended strength and duration when deciding review frequency.
- Pred Forte's UK SmPC requires strict ophthalmic supervision and regular pressure checks when treatment extends beyond ten days; this does not imply that shorter treatment is risk-free.
- Discuss reduction, substitution or withdrawal with the responsible prescriber and treat pressure as required; do not abruptly stop essential graft, uveitis or systemic steroid treatment.
- Following Ozurdex, early injection checks do not replace later pressure surveillance because a steroid-related rise can develop weeks after treatment.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Ocular corticosteroid exposure
Drops and ointments used on the eye, periocular injections and sustained intravitreal preparations can expose the trabecular pathway to corticosteroid effects. Higher potency or prolonged exposure can increase concern in susceptible patients.
Systemic and other routes
Oral and other non-ocular corticosteroid treatment can be relevant to pressure elevation. A complete history includes inhaled, nasal and periocular skin preparations, recognising that systemic absorption and ocular exposure differ between routes.
Individual susceptibility
A previous steroid pressure response, established glaucoma or a relevant family history strengthens the need for a considered monitoring plan. Age, comorbidity and the underlying eye disease also influence assessment.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Reduced trabecular outflow
Corticosteroid effects on trabecular cells and extracellular material can increase resistance to aqueous drainage through an otherwise open angle, raising the pressure needed to maintain fluid outflow.
- 2Silent pressure exposure
A gradual pressure rise may cause no pain and leave central visual acuity initially intact. Without measurement, an affected person may continue treatment while the optic nerve experiences sustained additional stress.
- 3Potential reversibility of pressure
Pressure often falls after the causative exposure is reduced or stopped, but the course varies with preparation, duration and pre-existing disease. Established ganglion-cell loss is not reversed by subsequent pressure normalisation.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
An asymptomatic pressure increase after starting or intensifying steroid treatment is a common route to detection; compare with baseline and examine for competing mechanisms.
Cells, flare or synechiae suggest that inflammatory obstruction may coexist with steroid response, requiring a specialist plan for both processes.
Blurred vision, ocular discomfort, haloes or headache warrant assessment, with urgent escalation for severe pain or rapid deterioration rather than assuming a harmless treatment effect.
Repeated steroid prescriptions without a documented indication, duration, pressure assessment or responsible eye service should trigger clarification and coordinated review.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Pressure measurement with anterior segment assessmentFirst step - Why
- Confirm the rise and look for its mechanism and current severity.
- Interpretation and limitations
- Use appropriate tonometry and examine for inflammation, corneal change and angle abnormalities; compare both eyes and previous readings where available.
- 02
Chronological steroid and ocular history - Why
- Relate the pressure change to exposure and identify prior susceptibility.
- Interpretation and limitations
- Record the preparation, route, frequency, start date, recent increases and any depot or implant treatment; include the disease being treated and past steroid responses.
- 03
Gonioscopy, disc assessment and appropriate imaging - Why
- Classify the angle and identify existing pressure-related nerve injury.
- Interpretation and limitations
- An open angle supports a typical steroid outflow mechanism but does not exclude mixed disease; rim or nerve-fibre damage changes the urgency and long-term target.
- 04
Visual fields and assessment of alternative visual causes - Why
- Measure functional impact and investigate symptoms not explained by pressure alone.
- Interpretation and limitations
- Perform reliable perimetry when practical and assess the lens, cornea and macula as indicated; a pressure response and another cause of visual loss may coexist.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Inflammatory pressure elevation
Active trabeculitis, inflammatory debris, synechiae or pupil block can raise pressure in an eye receiving steroids for uveitis. The treatment history does not by itself prove that the steroid is the only cause.
Pre-existing glaucoma or ocular hypertension
Previously unrecognised pressure-related disease may be discovered during steroid monitoring. Earlier records, the extent of nerve damage and the response to exposure changes help interpret the relationship.
Other steroid-related visual disorders
Cataract, corneal infection and central serous chorioretinopathy can cause visual symptoms during steroid treatment. A normal pressure reading should not end investigation of persistent new visual disturbance.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01Prevention and detectionPlan surveillance around the steroid exposureFirst stepA steroid course is being started, intensified or continued in a person with potential ocular risk.+
- 1Record the indication and expected duration, review previous pressure responses and glaucoma history, and establish baseline ocular information appropriate to the planned treatment.
- 2Agree who will check pressure and when, taking account of formulation, intensity, patient risk and the relevant SmPC rather than applying a generic annual interval.
- 3Explain the possibility of a silent rise and provide an urgent contact route for visual symptoms, confirming that repeat prescribing remains linked to the review plan.
02Detected pressure riseProtect vision while reassessing steroid needPressure increases during corticosteroid treatment or optic nerve damage is detected.+
- 1EscalationArrange ophthalmic assessment of severity, angle, nerve status and active inflammation, escalating immediately when symptoms or pressure threaten vision.
- 2Discuss reducing potency or frequency, substituting treatment or tapering when clinically safe with the original prescriber; avoid unilateral abrupt withdrawal of essential therapy.
- 3Start suitable pressure-lowering treatment when indicated and set a specific response review, considering laser or surgery if adequate control cannot otherwise be maintained.
03Persistent or prolonged exposureMaintain a coordinated longer-term planThe steroid cannot be stopped, a depot remains active or pressure stays elevated after adjustment.+
- 1Document the continuing steroid indication and expected exposure, and agree the pressure target with the relevant glaucoma and treating specialty teams.
- 2Monitor structure, function and pressure over time, adjusting hypotensive therapy and revisiting steroid-sparing options where appropriate for the underlying disease.
- 3Communicate the steroid response prominently before future courses or injections so subsequent prescribers can choose and monitor treatment with this history in view.
Key medicines and prescribing safety1 treatment · regimens, roles and cautions+
Dorzolamide 20 mg/mL for suitable pressure reduction
The selected dorzolamide product uses a single drop in each affected eye three times a day when prescribed alone, or twice a day as adjunctive therapy to an ophthalmic beta-blocker; continue to the specified pressure review.Check renal function where relevant: creatinine clearance below 30 mL/min and hyperchloraemic acidosis preclude use. Consider serious sulphonamide-type reactions and corneal disease, avoid routine combination with oral carbonic anhydrase inhibitors, and leave at least ten minutes between this product and other topical eye medicines.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Irreversible optic nerve loss
Prolonged uncontrolled pressure can lead to rim and nerve-fibre loss with corresponding field defects. The aim of early detection is to prevent this transition from a pressure response to permanent glaucoma.
Loss of inflammatory control
Unplanned steroid withdrawal can allow recurrence of uveitis or threaten a corneal graft, while abrupt interruption of prolonged systemic therapy can cause additional systemic harm. Pressure management must preserve necessary disease control.
Persistent treatment requirement
Some patients continue to need pressure-lowering medication, laser or surgery after steroid adjustment, especially with established glaucoma or a prolonged-release preparation whose exposure cannot be ended immediately.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- For topical Pred Forte, pressure should be checked frequently; use beyond ten days requires strict ophthalmic supervision with regular pressure measurement, and the individual review may need to occur earlier.
- For long-term systemic corticosteroid monitoring, the July 2026 SPS guidance includes baseline eye examination and examination every 6–12 months once stable; a known responder, active ocular treatment or new symptoms needs a more specific plan.
- Ozurdex's SmPC describes immediate optic nerve perfusion assessment, pressure measurement within 30 minutes and biomicroscopy at 2–7 days as possible early monitoring, with regular later pressure checks irrespective of baseline pressure.
- After steroid reduction or withdrawal, demonstrate that pressure has settled and review whether hypotensive treatment remains necessary; do not stop glaucoma medication solely because the steroid prescription has ended.
- Continue longer-term nerve and field assessment when damage has occurred, and record a prior steroid response for future prescribing decisions.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Early injection checks answer a different question
An immediate post-injection pressure check addresses the procedure's early consequences. A later steroid response can develop despite a reassuring first visit. In Ozurdex studies, the largest proportion of substantial rises occurred around 45–60 days; this supports continued surveillance without imposing that period as the only time a rise can occur.
An implant cannot simply be omitted tomorrow
A sustained-release preparation continues to expose the eye after administration. The retina or uveitis team should assess glaucoma suitability before treatment; Ozurdex is contraindicated in advanced glaucoma that cannot be controlled adequately by medicines alone. A later pressure response requires specialist management rather than an instruction to stop taking an implanted dose.
Children need an individual plan
Difficulty obtaining a pressure reading does not remove the risk, and children may need adapted assessment and closer specialist supervision. Prolonged frequent high-dose ocular steroids can also produce systemic effects, including adrenal suppression. Paediatric use and any pressure medicine must follow age-appropriate specialist prescribing rather than a copied adult regimen.
A lower-potency steroid is not universally interchangeable
Changing preparation may reduce pressure burden in selected cases, but anti-inflammatory efficacy and penetration also change. The appropriate substitute depends on the original indication, including corneal transplantation or uveitis. The clinician controlling that disease should participate in the decision and define the response and recurrence checks.
Shared prescribing requires shared information
The Greater Manchester ophthalmic steroid guidance places monitoring within a communicated specialist plan. If a scheduled review has been missed, the prescriber should urgently contact the responsible service to restore review; withholding a necessary established steroid solely because correspondence is delayed can itself cause harm.
11Common pitfallsFrequent interpretation and management errors.
- 01
Waiting for eye pain before measuring pressure during a prolonged topical steroid course.
- 02
Assuming every pressure rise in a treated uveitic eye is a pure steroid response.
- 03
Using a general systemic-steroid six-to-twelve-month eye interval for a new high-risk ocular steroid exposure.
- 04
Abruptly stopping essential steroid treatment without discussing inflammation, graft protection or systemic consequences.
- 05
Ending surveillance after a normal immediate post-injection pressure or after the last prescribed steroid dose.