01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Primary open-angle glaucoma describes an optic neuropathy in an eye whose drainage angle remains open and where a specific secondary cause has not been identified. Retinal ganglion cells and their axons are progressively lost, changing the neuroretinal rim and nerve-fibre layer and eventually the field of vision. The diagnosis rests on evidence of damage rather than the pressure number alone. Ocular hypertension is a related risk state in which pressure is repeatedly raised but the optic nerve and visual field do not show glaucoma.
Most people do not notice early disease. The fellow eye and remaining field can compensate, while central acuity may remain good despite meaningful peripheral damage. Ask about family history, prior eye findings, steroid exposure, trauma and previous ocular operations. Increasing age and a family history affect suspicion, but risk factors cannot substitute for examination. Explain why an asymptomatic person may still need monitoring or treatment without suggesting that an elevated reading inevitably causes blindness.
Pressure is a modifiable contributor to damage, but susceptibility varies between individuals and between eyes. Some optic nerves deteriorate at measurements conventionally regarded as normal. Conversely, another person may have persistent ocular hypertension without developing clinically important damage during their remaining lifetime. The treatment target therefore combines baseline damage, anticipated rate of change, life expectancy and treatment burden. A pressure described as normal on a laboratory-style range is not automatically an adequate target for advanced disease.
Diagnostic assessment brings together Goldmann applanation tonometry, a stereoscopic optic-disc examination, automated perimetry, gonioscopy and corneal thickness. Record a baseline image that can later be compared directly. Corneal properties and prior refractive surgery affect interpretation of pressure; do not simply add or subtract an arbitrary correction from a chart. Gonioscopy helps distinguish an open angle from closure and may reveal pigment, pseudoexfoliative material or other clues that change the diagnosis.
The NICE referral threshold of 24 mmHg is a case-finding rule, not a definition of glaucoma. A repeatable glaucomatous field defect or suspicious nerve damage warrants referral even at lower pressure. In a stable asymptomatic person, repeating an uncertain field or pressure on another occasion can reduce false-positive referrals. This is inappropriate when the clinical situation is urgent. Send the actual test results, photographs when available, previous measurements and relevant history so the receiving service can judge priority.
Initial treatment should be discussed with the person in terms of preserving useful vision. NICE offers 360-degree selective laser trabeculoplasty to eligible newly diagnosed non-advanced chronic open-angle glaucoma. For ocular hypertension, the same offer requires pressure of at least 24 mmHg and meaningful lifetime risk. Pigment dispersion-associated cases are excluded from these initial laser recommendations. Laser can reduce dependence on drops, but its effect can wane and it does not remove the need for follow-up.
A generic prostaglandin analogue is an appropriate initial medicine when laser is declined, unsuitable, needed treatment cannot await laser, or laser alone has not achieved enough reduction. Latanoprost is usually given once daily in the evening. Demonstrate administration and ask the person to show the technique; an unopened bottle or a drop repeatedly landing on the cheek cannot have its intended effect. For advanced chronic open-angle glaucoma, NICE recommends offering glaucoma surgery with antiscarring augmentation as indicated and discussing its benefits and risks. Offer interim generic prostaglandin treatment when surgery is planned.
Follow-up assesses preservation of function as well as pressure. An apparently successful fall in pressure cannot overrule reliable evidence that the disc or visual field is worsening. Reconsider the target, treatment delivery and diagnosis if these findings diverge. Also ask about ocular irritation, daily routines, medicine supply, cognition and dexterity. A sustainable regimen and a clearly assigned review date are essential parts of treatment, particularly when the immediate benefit cannot be felt.
Key points
- Glaucoma is progressive optic nerve damage with corresponding structural or functional loss; ocular hypertension describes raised pressure without established glaucomatous damage.
- A pressure within the usual population range does not exclude glaucoma, and an isolated high reading does not establish optic neuropathy.
- Assess the optic discs, visual fields, angle and Goldmann applanation pressure; measure central corneal thickness during diagnostic assessment.
- Consider repeat pressure and field testing before routine referral, but refer for disc damage, a consistent glaucomatous field defect or Goldmann-type pressure of at least 24 mmHg.
- Offer 360-degree selective laser trabeculoplasty for eligible newly diagnosed non-advanced open-angle glaucoma; the NICE initial laser recommendation excludes pigment dispersion-associated cases.
- For newly diagnosed ocular hypertension, the NICE laser offer requires pressure at least 24 mmHg and risk of visual impairment within the person's lifetime.
- Generic prostaglandin drops are appropriate when laser is declined, unsuitable, awaited with interim treatment needed, or insufficient; offer glaucoma surgery for advanced disease, with antiscarring augmentation when indicated.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Primary susceptibility
Ageing, inherited susceptibility and individual optic nerve characteristics contribute to primary disease; a family history raises suspicion without identifying a single sufficient cause in most affected adults.
Persistent pressure elevation
Reduced aqueous drainage through an anatomically open outflow pathway can raise pressure, producing ocular hypertension before demonstrable nerve damage or accompanying established glaucoma.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Outflow resistance
Aqueous continues to leave the anterior chamber through an open angle, but increased resistance in the trabecular pathway can elevate the pressure required to maintain drainage.
- 2Axonal injury
Mechanical and vascular influences at the optic nerve head contribute to retinal ganglion-cell axon loss, with individual susceptibility determining the relationship between measured pressure and damage.
- 3Loss of visual function
Damage follows the organisation of retinal nerve-fibre bundles, producing local field defects that can enlarge and eventually threaten fixation and everyday visual tasks.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Disc rim thinning, focal notching or a nerve-fibre defect may be discovered during examination despite the absence of pain or a subjective complaint.
A repeatable arcuate defect, nasal step or paracentral abnormality should be related to the disc appearance and test quality before assigning significance.
Repeatedly elevated pressure with normal disc and reliable fields describes a risk state requiring assessment of future visual impairment rather than automatic glaucoma labelling.
Marked pallor, sudden loss, reduced colour perception or neurological symptoms should prompt investigation beyond the usual chronic glaucoma pathway.
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
Goldmann applanation and repeat measuresFirst step - Why
- Establish pressure with an appropriate method and assess reproducibility.
- Interpretation and limitations
- Compare with earlier readings and consider corneal and treatment factors; non-contact pressure alone should not determine a routine referral.
- 02
Stereoscopic disc examination and OCT - Why
- Document neuroretinal rim and nerve-fibre structure at baseline.
- Interpretation and limitations
- Interpret images alongside actual disc size and appearance; a database colour classification cannot independently diagnose or exclude glaucoma.
- 03
Standard automated perimetry - Why
- Measure functional loss and define a reproducible baseline.
- Interpretation and limitations
- Assess reliability and repeat uncertain abnormalities; a defect should be anatomically plausible and interpreted with structural findings.
- 04
Gonioscopy and central corneal thickness - Why
- Classify the drainage angle and contextualise pressure measurement.
- Interpretation and limitations
- Gonioscopy identifies closure or secondary clues; corneal thickness contributes to risk assessment without supporting an arbitrary universal pressure correction.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Physiological large cups
A large optic disc may contain a relatively large normal cup; stable rim tissue, nerve-fibre measurements and reproducible visual fields help distinguish anatomy from progressive disease.
Secondary open-angle disease
Steroid exposure, pigment dispersion, pseudoexfoliation or previous trauma may increase outflow resistance while the angle remains open, requiring attention to the underlying cause.
Non-glaucomatous optic neuropathy
Disproportionate pallor, impaired colour vision, an atypical field pattern or rapid visual deterioration suggests another optic nerve disorder and may require neuro-ophthalmic investigation.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01Case findingConfirm the referral indicationFirst stepA routine eye assessment identifies raised pressure or possible glaucomatous damage.+
- 1Assess the disc, fields and angle and obtain Goldmann-type pressure measurements before deciding the routine referral pathway.
- 2Repeat uncertain measurements when clinically appropriate, while bypassing repeat-measure pathways if symptoms or severity require urgent assessment.
- 3Refer for disc damage, a glaucomatous field defect or pressure of at least 24 mmHg, supplying the findings and previous results.
02Initial managementMatch treatment to lifetime riskSpecialist assessment confirms ocular hypertension or newly diagnosed open-angle glaucoma.+
- 1Separate isolated pressure elevation from established damage and agree the likely lifetime visual risk and intended treatment target.
- 2Discuss eligible 360-degree SLT and its limitations; choose a generic prostaglandin analogue when laser is declined, unsuitable, awaited or insufficient.
- 3For advanced disease, offer glaucoma surgery with appropriate augmentation, discuss benefits and risks, and provide interim generic prostaglandin treatment while surgery is arranged.
03EscalationRespond to insufficient protectionEscalationPressure remains above the intended target or reliable structure or field results show progression.+
- 1Check actual drop delivery, adherence, tolerability and interacting medicines before interpreting the response as pharmacological failure.
- 2Reassess the target and consider another drug class, laser or augmented glaucoma surgery with the responsible glaucoma clinician.
- 3EscalationDocument the revised treatment and reassessment interval, ensuring the patient understands why escalation is needed despite minimal symptoms.
Key medicines and prescribing safety1 treatment · regimens, roles and cautions+
Latanoprost 50 micrograms/mL eye drops
Instil one drop into each affected eye once daily, preferably in the evening; continue long term until the glaucoma team changes or stops treatment.Do not exceed once-daily dosing or duplicate prostaglandin analogues. Discuss iris pigmentation and ocular irritation; use specialist judgement with uveitis, herpetic keratitis or macular-oedema risk. The cited Xalatan SmPC advises against pregnancy use and requires avoiding breastfeeding exposure or stopping breastfeeding after a coordinated treatment decision.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Progressive field restriction
Established ganglion-cell loss is irreversible, and further damage can compromise mobility, reading, driving eligibility and independence even before central acuity becomes markedly reduced.
Treatment intolerance
Long-term topical exposure may cause ocular surface symptoms or systemic adverse effects, reducing adherence and complicating the ability to maintain the intended pressure reduction.
Late recognition
Initially silent disease can reach an advanced stage before detection, leaving little functional reserve and a narrower margin for further progression or missed follow-up.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Track pressure alongside reproducible fields and optic nerve change, using previous images and results rather than assessing each visit in isolation.
- Set the next appointment according to control, risk and uncertainty; a stable treated ocular-hypertension schedule cannot be applied automatically to progressive glaucoma.
- Ask about symptoms from treatment, medicines supply and practical difficulties, and observe drop technique when response or adherence is uncertain.
- Review the better-seeing eye and the person's functional priorities, arranging support or visual rehabilitation when field loss affects daily activities.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Normal pressure can coexist with glaucoma
The population distribution of pressure does not define an individual nerve's tolerance, so convincing structural and field damage needs assessment even below referral pressure thresholds.
Do not promise restoration
Pressure reduction aims to limit future loss; existing ganglion-cell damage is not reversed by a good tonometry result.
Laser does not end surveillance
An initially effective laser response may diminish over time and requires the same attention to function and later treatment need.
Risk is measured over years
Treatment decisions for ocular hypertension balance the chance of future impairment with remaining lifetime and burdens, without equating every raised reading with inevitable blindness.
11Common pitfallsFrequent interpretation and management errors.
- 01
Using the 24 mmHg referral threshold to dismiss a damaged optic nerve with lower pressure.
- 02
Starting several drops before establishing whether the drainage angle is open and whether a secondary cause is present.
- 03
Repeating an air-puff reading alone instead of obtaining appropriate case-finding tests and referral information.
- 04
Assuming that no symptoms or preserved reading acuity makes established field loss unimportant.