Secondary glaucoma

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Secondary glaucoma is a mechanistic diagnosis as well as a pressure problem. A recognisable process alters aqueous drainage or anterior segment anatomy and produces damage to the optic nerve. The process may be quiet, as with pseudoexfoliation, or acutely painful, as with neovascular angle closure. Establishing whether the angle is open, partly scarred or closed determines which interventions can work.

A useful assessment asks three questions: what is happening to the pressure, what is causing the outflow disturbance, and how much useful vision is threatened? These questions prevent two common errors: assuming an open angle means primary disease, and treating the measured pressure without addressing active inflammation or retinal ischaemia. Different services may need to work together. A patient receiving retinal injections, for example, may require both a retinal plan for the ischaemic drive and a glaucoma plan for an already damaged drainage pathway.

Key points

Secondary glaucoma means optic nerve injury associated with an identifiable ocular disease, treatment or injury; isolated secondary ocular hypertension does not yet establish glaucoma.
Inspect the cornea, iris, lens and angle as well as the optic nerve; pressure measurement alone cannot identify the cause.
Pigment dispersion and pseudoexfoliation can obstruct outflow while the angle remains open, whereas neovascular membranes or secondary displacement can close it.
Uveitic pressure elevation may reflect inflammation, adhesions, steroid response or several mechanisms together; inflammation must remain adequately treated.
For retinal vein occlusion with iris or angle new vessels, anti-VEGF treatment is an adjunct to prompt panretinal photocoagulation, with the retinal service defining timing.
Dorzolamide 20 mg/mL monotherapy is one drop in the affected eye three times daily; the selected SmPC reduces this to twice daily when added to an ophthalmic beta-blocker.
Review all routes of steroid exposure, previous trauma and eye surgery, and arrange continued optic nerve and field monitoring after the immediate cause is addressed.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Material within the drainage pathway

Pigment released from the iris and pseudoexfoliative material deposited within the anterior segment can increase trabecular resistance. The associated syndrome can exist before pressure elevation or glaucomatous nerve damage develops.

Inflammation and treatment exposure

Inflammatory cells, trabecular inflammation and adhesions can alter outflow during uveitis. Corticosteroids prescribed to control that inflammation may independently provoke a pressure response in susceptible eyes.

Ischaemia, injury and surgery

Retinal ischaemia may stimulate abnormal vessels and fibrovascular tissue in the angle. Trauma or ocular procedures can damage drainage structures, obstruct outflow with blood or displace the iris–lens relationship.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Secondary open-angle resistance
The anatomical angle remains visible, but pigment, exfoliative material, inflammatory debris or altered trabecular tissue impairs aqueous drainage. Continued pressure elevation can injure retinal ganglion-cell axons.
2
Neovascular obstruction and contraction
Ischaemia-driven vascular growth spreads onto the iris and angle, initially compromising drainage and later forming contracting fibrovascular tissue. Peripheral adhesions can convert an initially open angle into irreversible synechial closure.
3
Multiple mechanisms in one eye
An inflamed eye may have active trabeculitis, posterior synechiae, pupil block and a steroid response together. Treatment directed at only one element may fail despite apparently appropriate pressure-lowering medication.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Pigment or exfoliative deposits

Heavy angle pigmentation, iris pigment loss or flaky material around the pupil and lens suggests a secondary open-angle mechanism requiring targeted anterior segment examination.

Inflammatory signs with high pressure

Cells, flare, keratic precipitates or synechiae in a painful photophobic eye suggest uveitic disease; note whether steroid treatment preceded or followed the pressure rise.

Rubeosis and retinal ischaemia

Fine abnormal vessels at the pupil margin or within the angle, particularly after ischaemic retinal disease, demand urgent assessment before further synechial closure develops.

Asymmetric or delayed post-traumatic disease

Unilateral pressure elevation with a history of blunt injury should prompt careful gonioscopy and review of old records, even when the original injury is no longer symptomatic.

Red flags requiring action

A painful high-pressure eye with iris neovascularisation after retinal vein occlusion or proliferative diabetic retinopathy needs urgent retinal and glaucoma assessment to address both ischaemia and pressure.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

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, acuity and urgent anterior segment examinationFirst step
Why
Assess current threat and identify a painful secondary emergency.
Interpretation and limitations
Document both eyes and examine for corneal oedema, inflammation, new vessels or lens abnormality; in recent trauma, exclude an open globe before applying pressure to the eye.
02
Gonioscopy with targeted anatomical assessment
Why
Determine whether the angle is open, obstructed, recessed or synechially closed.
Interpretation and limitations
Look for angle vessels, abnormal pigmentation and scarring; the mechanism cannot be inferred reliably from the pressure level or a normal-looking central chamber alone.
03
Dilated retinal examination and indicated retinal imaging
Why
Identify ischaemia, vein occlusion, diabetic changes or another posterior segment cause.
Interpretation and limitations
Retinal assessment informs treatment of the angiogenic stimulus; macular imaging evaluates a separate cause of visual loss and does not replace examination for iris or angle neovascularisation.
04
Optic nerve imaging, fields and exposure chronology
Why
Stage glaucomatous damage and relate pressure changes to possible causes.
Interpretation and limitations
Establish reliable baselines once acute media opacity and pain permit; compare steroid courses, injuries and procedures with previous pressure values rather than assuming a coincidental exposure is causal.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Primary open-angle glaucoma

A primary diagnosis requires appropriate examination for secondary clues. Marked asymmetry, unusual age of onset, inflammation, abnormal angle pigmentation or a relevant ocular history should prompt reconsideration.

Secondary ocular hypertension

High pressure without demonstrable optic nerve or field damage is a risk state rather than established glaucoma. It may still require urgent treatment when the pressure, cause or threatened tissue makes delay unsafe.

Non-glaucomatous visual loss

Retinal ischaemia, macular oedema, cataract or corneal disease may explain reduced acuity alongside raised pressure. The extent of vision loss should not automatically be attributed entirely to optic neuropathy.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Cause identificationClassify the secondary outflow problemFirst stepRaised pressure or optic neuropathy is accompanied by an unusual ocular history or anterior segment finding.

1Assess immediate visual threat and examine the angle and anterior segment for pigment, exfoliation, inflammation, vessels and structural injury.
2Review medicines, including non-ocular steroids, and obtain the timing of trauma, surgery, retinal events and previous pressure measurements.
3Record the likely mechanism and damage stage, then arrange glaucoma care with the additional retinal, uveitis or surgical service needed to treat the cause.

02Neovascular diseaseControl pressure and the retinal stimulusIris or angle neovascularisation appears in an eye with retinal ischaemia or a painful pressure rise.

1Obtain urgent ophthalmic assessment of remaining visual potential, angle closure, pressure and the underlying retinal ischaemia.
2Coordinate anti-VEGF treatment with sufficient panretinal photocoagulation; in vein occlusion, the RCOphth recommendation places laser on the same day before injection or within one to two weeks.
3Use appropriate pressure medication and consider drainage surgery or cycloablation when indicated; continue surveillance because vessel regression after an injection does not prove durable control.

03Inflammatory or treatment-related diseaseBalance inflammation and pressure treatmentPressure elevation occurs during uveitis or exposure to corticosteroids.

1Establish whether active inflammation, adhesions, a steroid response or mixed disease best explains the findings, including consideration of infectious uveitis.
2Discuss steroid adjustment with the responsible eye team and treat pressure concurrently; do not abruptly remove necessary anti-inflammatory or systemic steroid treatment.
3EscalationReview the response promptly and escalate treatment when the nerve remains at risk, maintaining a separate plan for recurrence of the underlying inflammatory disease.

Key medicines and prescribing safety1 treatment · regimens, roles and cautions

Topical aqueous suppression for a suitable secondary open-angle glaucoma, including the licensed pseudoexfoliative indication.

Dorzolamide 20 mg/mL eye drops

Use one drop in each treated eye three times daily as monotherapy; when used as an adjunct to an ophthalmic beta-blocker, the selected product specifies one drop twice daily. Continue until a planned pressure review or a revised prescription.

Contraindicated with creatinine clearance below 30 mL/min or hyperchloraemic acidosis. Review sulphonamide-type hypersensitivity, renal calculi and compromised corneal endothelium; concurrent oral carbonic anhydrase inhibitor treatment is not recommended by this SmPC. Separate other topical eye medicines by at least ten minutes.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Combined retinal and nerve damage

Neovascular glaucoma may coexist with severe retinal ischaemia, limiting visual recovery even when pressure is controlled. Prognosis requires assessment of both retinal function and remaining optic nerve reserve.

Irreversible drainage scarring

Inflammatory or neovascular synechiae can persist after active disease subsides. Long-term medication or glaucoma surgery may be necessary because removal of the initiating stimulus does not reopen a permanently scarred angle.

Persistent ocular discomfort

Severely damaged eyes can develop recurrent pressure-related pain and corneal changes. When useful vision cannot be recovered, a documented comfort-focused ophthalmic plan still requires active treatment and follow-up.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Monitor the underlying disease alongside pressure: recurrence of inflammation or neovascularisation can precede another deterioration in glaucoma control.
Use reproducible disc and field assessments after acute stabilisation to distinguish persistent optic nerve injury from reversible blur caused by corneal or macular changes.
Recheck the medication list at transitions between retina, uveitis, glaucoma and primary care, especially when steroid doses or fixed-combination drops change.
Set follow-up according to the active mechanism and visual reserve; a stable primary ocular-hypertension interval is inappropriate for evolving neovascular or postoperative disease.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Pigment dispersion is a syndrome before glaucoma

Pigment findings alone do not establish nerve damage. Patients may need observation, treatment for elevated pressure or glaucoma therapy depending on the pressure trend and structural and functional assessment.

Laser eligibility needs specific judgement

NICE excludes pigment dispersion-associated cases from its routine initial 360-degree SLT offer. This is not a universal prohibition on expert-selected laser treatment; pigmentation and post-laser pressure risk require individual consideration.

Pseudoexfoliation matters during cataract planning

Deposits may accompany zonular weakness and instability of the lens. Communicating their presence helps the surgeon anticipate lens-support difficulties while planning pressure and visual rehabilitation.

The therapeutic target can change

An apparently successful treatment of the precipitating condition may leave substantial optic nerve vulnerability. Reassess the acceptable pressure and monitoring frequency rather than assuming the original target remains adequate.

11Common pitfallsFrequent interpretation and management errors.

01
Calling a deeply pigmented or scarred angle primary disease without investigating secondary features.
02
Treating neovascular glaucoma solely with drops while the ischaemic retinal stimulus remains active.
03
Stopping necessary steroid treatment abruptly because pressure is raised, without addressing ongoing inflammation or systemic risk.
04
Interpreting temporary regression of iris vessels after anti-VEGF treatment as proof that retinal laser and surveillance are unnecessary.