Glaucoma can destroy half your optic nerve before you notice anything wrong. Half. It is not a condition you can feel coming. That is exactly why regular eye examinations save sight.

Glaucoma is a group of conditions in which the optic nerve, the cable that carries visual information from the eye to the brain, is progressively damaged. As nerve fibres are lost, the visual field gradually shrinks, typically starting from the periphery and working inward. The most common form causes no pain, no redness, and no noticeable change in vision until a great deal of damage has already occurred. Glaucoma is the leading cause of irreversible blindness worldwide. The nerve damage it causes cannot be undone, but with early detection and consistent treatment it can almost always be halted or slowed enough to preserve functional vision for life. Specialist care is provided by the glaucoma subspecialty page.

What You Need to Know About Glaucoma

Most glaucoma causes no symptoms until significant and permanent nerve damage has occurred. Regular eye examinations are the only reliable way to detect it early
Elevated intraocular pressure (IOP) is the main risk factor and the primary target of all treatments
Glaucoma cannot be cured, but it can be controlled: treatment prevents further damage rather than restoring what has been lost
First-degree relatives of people with glaucoma have a 4 to 9 times higher risk and should have regular eye examinations from their 40s
Treatment must be continued for life. Stopping drops, even when vision feels completely normal, allows pressure to rise and damage to continue
Most people with well-managed glaucoma retain good functional vision throughout their lives

Silent damage 40% Of optic nerve fibres can be lost before vision changes are noticeable

Family history risk 4-9x Higher risk with a first-degree relative with glaucoma

Global burden No. 1 Cause of irreversible blindness worldwide

What Happens to the Optic Nerve

The optic nerve is made up of around 1.2 million nerve fibres, each carrying visual information from a specific point on the retina. In glaucoma, these fibres are progressively lost. The nerve head, where the optic nerve exits the eye, has a central cup surrounded by a rim of healthy nerve tissue. As fibres are lost, this cup enlarges and the rim thins. The ratio between cup size and disc size, the cup-to-disc ratio, is one of the key measurements ophthalmologists track.

Side-by-side fundus photographs comparing a normal optic disc on the left with a small central cup versus a glaucomatous disc on the right with a large excavated cup and thin remaining rim — Left: normal optic disc with a small cup and healthy rim. Right: glaucomatous disc with a markedly enlarged cup and a thin, compromised rim indicating significant nerve fibre loss.

Because the peripheral nerve fibres are typically lost first, and because the brain is remarkably good at compensating for gradual change, most patients don’t notice their visual field shrinking until it has contracted substantially. By the time a person is aware that something is wrong with their peripheral vision in daily life, they may have already lost 40 percent or more of their optic nerve fibres. This is what makes glaucoma so dangerous: it has usually been present for years before it is felt.

Types of Glaucoma

Primary open-angle glaucoma

Primary open-angle glaucoma (POAG) is the most common type, accounting for around 90 percent of glaucoma in Western populations. The drainage angle of the eye remains anatomically open but drains inefficiently. Aqueous humour gradually builds up, raising intraocular pressure (IOP). The elevated pressure slowly damages the optic nerve over months and years, with no pain and no warning. It can progress for years without being detected unless eye examinations include optic nerve assessment and IOP measurement.

Normal tension glaucoma is a form of POAG in which optic nerve damage progresses despite IOP readings within the statistically normal range. The optic nerve appears unusually vulnerable to pressure even at levels that don’t damage most people’s nerves. The treatment approach is the same: lower the IOP further, and progression slows. Counterintuitive if the pressure was “normal” to begin with, but it works.

Primary angle-closure glaucoma

Angle-closure glaucoma occurs when the drainage angle of the eye is physically narrowed or blocked by the iris. It is more common in people with small, crowded eyes, in women, and in people of East and South Asian ancestry. Chronic angle closure progresses silently like open-angle glaucoma. Acute angle closure is different entirely: a medical emergency in which IOP rises to very high levels within hours, causing severe eye pain, headache, nausea, vomiting, blurred vision, and halos around lights. People with narrow angles can be treated preventively with a laser procedure (peripheral iridotomy) before acute closure occurs.

Secondary glaucomas

Secondary glaucomas develop as a consequence of another eye condition or systemic factor. Common causes include pseudoexfoliation syndrome, pigment dispersion syndrome, uveitis, trauma, neovascular glaucoma from diabetic retinopathy or retinal vein occlusion, and prolonged corticosteroid use. Steroid-induced glaucoma is underrecognised: any patient using steroid eye drops regularly should have their IOP monitored. See our steroids in eye care page for more on this.

Risk Factors

Elevated intraocular pressure

Raised IOP is the strongest known risk factor for glaucoma and the primary target of treatment. Normal IOP is generally considered to be between 10 and 21 mmHg, but this is a statistical definition rather than a safe threshold for every individual. An IOP that causes no damage in one person may cause significant optic nerve damage in another whose nerve is more vulnerable.

Age, family history, and ethnicity

POAG affects around 2 percent of people over 40 and rises to around 10 percent over 80. Having a first-degree relative with POAG increases personal risk by four to nine times. People of African or Caribbean ancestry have a three to four times higher risk than white Europeans, tend to develop it younger, and often have a more aggressive course. People of East and South Asian ancestry have elevated risk of angle-closure glaucoma.

High myopia

Severe short-sightedness (myopia greater than minus 6 dioptres) is an independent risk factor for POAG. The highly stretched optic nerve head and the altered anatomy of the myopic eye increase vulnerability to pressure-related damage. People with high myopia should be monitored for glaucoma as part of their regular eye care.

Diagnosis and Monitoring

Intraocular pressure and optic nerve assessment

IOP is measured with a tonometer, most commonly by applanation tonometry at the slit lamp. A single reading is a snapshot: IOP fluctuates throughout the day. Elevated IOP alone does not diagnose glaucoma and must be combined with optic nerve assessment. OCT scanning measures the retinal nerve fibre layer thickness with micrometric precision, detecting thinning that can precede detectable visual field loss by months to years. Fundus photography documents the optic nerve head and allows comparison over time.

Visual field testing

Automated visual field testing maps the peripheral and central visual field, detecting the characteristic pattern of loss caused by glaucoma: arcuate scotomas, nasal steps, and in advanced disease progressive constriction of the remaining field. Serial tests over time are compared to detect statistically significant progression, which directly informs whether treatment needs to be intensified.

Visual field test result showing a nasal step defect characteristic of glaucoma with asymmetric loss across the horizontal midline — A visual field result showing a nasal step, a characteristic pattern of glaucomatous field loss. This kind of peripheral loss typically goes unnoticed in daily life until it is well established.

Treatment

All current glaucoma treatments lower intraocular pressure. This doesn’t reverse existing damage but slows or halts further progression. The target pressure is individualised based on the stage of disease, rate of progression, and the patient’s life expectancy.

water_drop

First line

Pressure-lowering eye drops

Eye drops are the most widely used first-line treatment. Prostaglandin analogues (latanoprost, bimatoprost, travoprost) are the most effective single agents, reducing IOP by 25 to 35 percent, used once daily at night. Beta-blockers, carbonic anhydrase inhibitors, alpha-2 agonists, and newer agents such as rho kinase inhibitors each work by different mechanisms and can be combined when a single agent is insufficient. Adherence to drops is one of the most important determinants of long-term outcome and one of the most commonly underestimated challenges in glaucoma management.

light_mode

Effective alternative

Selective laser trabeculoplasty (SLT)

SLT uses a low-energy laser to stimulate the trabecular meshwork cells and improve aqueous drainage. It is effective, safe, repeatable, and increasingly used as a first-line treatment rather than a second-line addition. The LIGHT trial demonstrated that SLT as first-line treatment achieved IOP control comparable to drops in most patients, with many remaining drop-free for years. Five minutes per eye in the clinic, well tolerated.

surgical

When needed

Surgery

When drops and laser are insufficient, surgery is considered. Trabeculectomy creates a new drainage channel from inside the eye to beneath the conjunctiva. Highly effective but requires careful postoperative management over weeks. Minimally invasive glaucoma surgery (MIGS) describes a group of newer, safer procedures with a more modest pressure-lowering effect but a much better safety profile, suitable for mild to moderate disease. Drainage implants (tubes) are used in complex or refractory cases.

Living With Glaucoma: What Patients Ask Most

Will I go blind? The vast majority of people diagnosed at a reasonably early stage who take their drops and attend appointments maintain functional vision for life. The risk of blindness is much higher in those diagnosed late, who don’t take their drops consistently, or who don’t attend regular monitoring.

Can I drive? Many people with glaucoma continue driving for years. Fitness to drive depends on the extent of visual field loss and whether it meets the legal standard. Your ophthalmologist is required to advise you if they believe your vision no longer qualifies. If you have any doubt, discuss it rather than assuming.

Does exercise, diet, or sleep position affect glaucoma? Vigorous exercise generally lowers IOP slightly and is beneficial. Sleeping with the affected eye pressed against a pillow can raise IOP in that eye. Inverted yoga positions raise IOP sharply during the posture and are best avoided. Drinking large volumes of fluid quickly can transiently raise IOP. None of these factors replace medical treatment, but they are worth knowing about.

Seek Emergency Care Immediately If You Have

Sudden severe pain in one eye, accompanied by headache and nausea or vomiting
Suddenly blurred vision with halos or rainbow rings around lights
A red, painful eye with reduced vision rather than simple irritation
Any of the above, especially if you have been told you have narrow angles

These symptoms describe acute angle-closure glaucoma, a medical emergency in which IOP rises to very high levels within hours. It can cause permanent severe vision loss if not treated urgently. Go directly to an emergency eye clinic or hospital emergency department. Acute angle closure is completely different from common painless open-angle glaucoma and requires immediate treatment.

Frequently Asked Questions About Glaucoma

I have been told my pressure is high but I don’t have glaucoma yet. What does this mean?
This is called ocular hypertension: elevated IOP without any detectable optic nerve damage or visual field loss at the time of testing. It’s a risk factor for glaucoma, not glaucoma itself. Whether to treat with drops depends on the level of pressure, your optic nerve appearance, corneal thickness, age, and other factors. Some people with ocular hypertension are monitored without treatment; others are treated to reduce the risk of conversion. Your ophthalmologist will discuss what makes sense for your specific situation.
My drops are making my eyes red and irritated. Can I stop?
Don’t stop without speaking to your ophthalmologist first. This comes up more often than you might think, and there’s almost always a better alternative. Even a short break allows IOP to rise and can cause further optic nerve damage. If a drop is causing side effects, there are almost always alternative agents or preservative-free formulations that are better tolerated. Preservative-free versions cause far less surface irritation and are available for most drop classes. Call the clinic if the symptoms are significant rather than waiting for your next scheduled appointment.
How often do I need to be seen?
That depends on the stability and severity of your glaucoma. Newly diagnosed patients and those with unstable or advanced disease are typically reviewed every three to four months. Stable, well-controlled early glaucoma may be reviewed every six to twelve months. Most guidelines recommend at least two visual field tests and two OCT scans per year for patients in active monitoring.
My pressure is normal on treatment. Can I reduce my drops?
The normal pressure is because the drops are working. Remove the drops, and the pressure goes back up. Reducing them without medical guidance allows IOP to rise and damage to resume. Some patients whose pressure is very well controlled over years, particularly after laser or surgery, may be able to reduce drops with careful monitoring. That decision should always be made with your ophthalmologist and followed by more frequent IOP checks to confirm pressure remains controlled.
Does what I eat or drink affect glaucoma?
Diet doesn’t have a major direct effect for most patients. A few practical things are worth knowing, though. Drinking large volumes of fluid quickly can transiently raise IOP. Caffeine raises IOP slightly for an hour or two after consumption, though habitual coffee drinkers develop tolerance. A diet rich in leafy green vegetables has been associated with modest benefits in some studies. Avoiding smoking is beneficial, as it worsens vascular supply to the optic nerve.
Should my children or siblings be tested?
Yes. First-degree relatives have a much higher risk and should have regular eye examinations including optic nerve assessment and IOP measurement from around age 40, or earlier if there’s any concern. Family history alone is sufficient reason for proactive monitoring. Tell your relatives. Encouraging them to have their eyes checked is genuinely one of the most useful things a glaucoma patient can do.

If you would like to learn more, the Centers for Disease Control and Prevention’s glaucoma page offers a clear overview of glaucoma, risk factors, and why regular eye exams matter, while the Glaucoma Research Foundation website provides more detailed patient-friendly information about testing, treatment, and living with glaucoma.

Glaucoma is a progressive optic neuropathy characterized by characteristic structural changes to the optic nerve head and retinal nerve fiber layer (RNFL), associated with corresponding visual field (VF) loss, in which intraocular pressure (IOP) is the primary modifiable risk factor. It is the leading cause of irreversible blindness globally, affecting an estimated 80 million people. Primary open-angle glaucoma (POAG) accounts for the majority of cases in most populations; primary angle-closure glaucoma (PACG) predominates in East and South Asian populations and carries a higher risk of acute presentation. Management is centered on IOP reduction , the only intervention with strong evidence for slowing progression , delivered through drops, laser, or surgery depending on disease stage, target IOP, and patient factors. Visual field loss, once established, does not recover.

Clinical Overview: Glaucoma

Classification: POAG (primary open-angle glaucoma) , open angle, no secondary cause, IOP may be normal (NTG, normal-tension glaucoma) or elevated; PACG (primary angle-closure glaucoma) , trabecular meshwork blocked by peripheral iris; Secondary glaucomas , PXF (pseudoexfoliation), pigment dispersion, uveitic, neovascular, traumatic, steroid-induced
IOP reference: Statistically normal is below 21 mmHg (mean 15.5 ± 2.5 mmHg in population studies). IOP above 21 mmHg is ocular hypertension (OHT) , not glaucoma unless disc/field changes exist. NTG has disc and field damage with IOP consistently below 21 mmHg.
Target IOP: Set individually based on baseline IOP, disc damage stage, and rate of progression. Typically 20-30% reduction from baseline for mild-moderate POAG; more aggressive targets (below 12-15 mmHg) for advanced or rapidly progressing disease.
First-line medical therapy: Prostaglandin analogue (PGA , latanoprost, bimatoprost, travoprost, tafluprost) once daily: 25-35% IOP reduction. Beta-blockers second-line or adjunct. CAIs (carbonic anhydrase inhibitors) and alpha-2 agonists as adjuncts. Fixed combinations improve adherence.
Laser: SLT (selective laser trabeculoplasty) , LiGHT trial: SLT first-line as effective as drops, with 74% of patients requiring no further treatment at 3 years and lower treatment cost. Laser iridotomy (YAG-LI) for PACG and angle-closure suspects.
Surgery: Trabeculectomy with MMC (mitomycin C) , gold standard for advanced or medically uncontrolled disease. MIGS (minimally invasive glaucoma surgery) for mild-moderate disease at time of cataract surgery.

Global prevalence ~80M People affected; leading cause of irreversible blindness

SLT success (LiGHT) 74% No further treatment needed at 3 years

POAG undiagnosed ~50% Of POAG cases are undiagnosed at any given time

Pathophysiology

The primary site of IOP-related damage is the lamina cribrosa , a fenestrated collagen plate through which retinal ganglion cell (RGC) axons exit the eye. Elevated IOP compresses the lamina, disrupting axoplasmic flow and causing RGC apoptosis. The RNFL , composed of RGC axons , thins as ganglion cells die. This produces the structural changes detectable on OCT (RNFL thinning, macular ganglion cell complex thinning) and the optic nerve head changes visible clinically (cup enlargement, rim thinning, disc hemorrhages, RNFL defects visible as wedge-shaped dark bands in the peripapillary retina).

Fundus photographs comparing normal optic disc with glaucomatous disc — Disc comparison: normal CDR with intact neuroretinal rim (left) vs inferior rim thinning and enlarged cup in POAG (right).

Why IOP is not the whole story: Approximately one third of POAG patients have IOP consistently below 21 mmHg (normal-tension glaucoma). Vascular factors , particularly nocturnal hypotension, impaired autoregulation, and vasospasm , appear to contribute to RGC loss in NTG. Central corneal thickness (CCT) affects Goldmann applanation tonometry (GAT) readings: thin corneas underestimate IOP, thick corneas overestimate. CCT below 555 µm is an independent risk factor for POAG conversion (OHTS trial).

Aqueous dynamics: Aqueous humor is produced by the ciliary body and drains through two routes: the conventional trabecular meshwork/Schlemm’s canal pathway (75-90%) and the uveoscleral pathway (10-25%). IOP-lowering drugs target different parts of this system. PGAs increase uveoscleral outflow. Beta-blockers, CAIs, and alpha-2 agonists reduce aqueous production. Rho kinase inhibitors (netarsudil) increase trabecular outflow.

Diagnosis and Staging

Optic disc assessment: The vertical cup-to-disc ratio (CDR) is a crude but widely used metric. More important are rim characteristics: the ISNT rule (Inferior rim ≥ Superior rim ≥ Nasal rim ≥ Temporal rim) , violations suggest glaucomatous damage. Disc hemorrhages (splinter hemorrhages at the rim margin) are highly specific for glaucoma progression , their presence warrants intensified monitoring or treatment escalation. Peripapillary RNFL defects are visible as wedge-shaped dark areas on red-free fundus photography.

OCT RNFL analysis: Quantifies peripapillary RNFL thickness against a normative database. Thinning below the 5th percentile (yellow/orange on the printout) suggests damage; below the 1st percentile (red) is likely significant loss. The macular ganglion cell complex (GCC) map provides additional structural data, particularly for early disease where RNFL changes may precede VF changes. Structural loss typically precedes functional loss by 5-10 years.

Humphrey Visual Field (HVF) staging: MD (mean deviation) on HVF quantifies overall field loss: 0 to -6 dB = mild, -6 to -12 dB = moderate, below -12 dB = severe. The Glaucoma Hemifield Test (GHT) compares superior and inferior hemifields , “outside normal limits” is a clinically significant flag. The VFI (Visual Field Index) tracks percentage of normal field remaining. Reliability indices (fixation losses, false positives, false negatives) must be checked before interpreting any VF.

Gonioscopy: Mandatory before diagnosis. Classifies the angle (Shaffer grading: grade 0-4, where 0 = closed, 4 = wide open). Distinguishes open-angle from closed-angle disease, identifies synechiae, pigment, PXF material, neovascularization, and trauma-related angle recession. Cannot be reliably omitted on the basis of clinical appearance.

Medical Management

Prostaglandin analogues (PGAs): First-line for POAG and OHT. Once-daily evening dosing. 25-35% IOP reduction. Latanoprost (Xalatan), bimatoprost (Lumigan), travoprost (Travatan), tafluprost (Saflutan, preservative-free). Preservative-free formulations for patients with ocular surface disease or frequent instillation burden. Side effects: conjunctival hyperemia, iris pigmentation (irreversible, mainly in hazel eyes), periorbital fat atrophy, hypertrichosis. Contraindicated in uveitic glaucoma and during pregnancy.

Visual field test showing nasal step defect in glaucoma — HVF nasal step from inferotemporal RNFL loss: superior arcuate scotoma respecting the horizontal raphe.

Beta-blockers: Timolol 0.25-0.5% twice daily (or once-daily gel). 20-25% IOP reduction. Contraindicated in asthma, COPD (use with caution), bradycardia, heart block. Systemic absorption significant , check pulse and respiratory history. Dorzolamide/timolol (Cosopt) and brinzolamide/timolol fixed combinations are widely used.

SLT (selective laser trabeculoplasty): 532 nm Q-switched Nd:YAG laser applied to trabecular meshwork over 180° or 360°. Mechanism: selectively targets pigmented trabecular cells, stimulating biological renewal of drainage. The LiGHT trial (2019) demonstrated SLT is as effective as drops as first-line treatment, with 74% of SLT patients requiring no drops at 3 years and superior health economics. SLT is repeatable (typically once, sometimes twice). It takes 4-6 weeks for full effect. Not effective in angle closure or very heavily pigmented angles.

Surgical Management

Trabeculectomy with MMC: Creates a controlled fistula through the sclera, bypassing the trabecular meshwork. MMC (mitomycin C) is applied intraoperatively to inhibit fibrosis at the bleb. Target IOP of 8-12 mmHg achievable. Complications: bleb failure (most common long-term complication), hypotony maculopathy, bleb-related infection (blebitis/endophthalmitis , lifetime risk approximately 1-2%). Requires intensive postoperative management (bleb massage, suture lysis, anti-fibrotics). Still the gold standard for advanced or refractory glaucoma. Tube implant surgery (Ahmed, Baerveldt) is an alternative, particularly for previously operated eyes or neovascular glaucoma.

MIGS (minimally invasive glaucoma surgery): A heterogeneous group of ab-interno procedures targeting the trabecular meshwork (iStent inject, Hydrus), suprachoroidal space (CyPass , withdrawn), subconjunctival space (XEN gel stent), or ciliary body (ECP). Generally safer than trabeculectomy with more modest IOP reduction. Appropriate for mild-moderate glaucoma at time of cataract surgery. Not a substitute for trabeculectomy in advanced disease needing low target IOP.

Monitoring and Progression Analysis

Rate of progression: The key clinical question is not just whether glaucoma is present but how fast it is progressing. The AGIS and CIGTS studies established that the rate of MD change (dB/year) on serial HVFs predicts visual disability. A rate of change more negative than -1.5 dB/year is considered fast progression. At least 5 reliable VF tests over 3-5 years are needed to establish trend. OCT structural progression (RNFL thinning on trend analysis) may detect progression earlier than VF.

Disc hemorrhages: The most underappreciated sign of active glaucoma progression. A single splinter hemorrhage at the disc margin , particularly inferotemporal , is a specific marker of current axonal damage and predicts future RNFL loss and VF deterioration. Disc hemorrhages occur in approximately 7% of POAG patients per year. Their presence warrants: IOP measurement (often normal in NTG), consideration of treatment escalation, and accelerated follow-up.

Clinical Decision Points

New POAG diagnosis, IOP 24 mmHg, mild disc change, early VF loss: Discuss SLT as first-line (LiGHT evidence). If drops preferred, start PGA. Set target IOP: typically 20% reduction from baseline in mild disease.
NTG (IOP below 21 mmHg with disc and field damage): Target IOP still matters , CNTGS trial showed 30% IOP reduction from already-normal IOP slows progression. Consider systemic vascular assessment (nocturnal hypotension, vasospasm). CA II inhibitors (dorzolamide) have proposed neuroprotective effects beyond IOP.
Disc hemorrhage found at routine review: Recheck IOP on multiple occasions. Consider treatment escalation regardless of IOP if rate of progression is fast. Accelerate VF and OCT review to 4-monthly.
Advanced glaucoma (MD below -12 dB), IOP 18 mmHg on maximum tolerated medical therapy: Refer for trabeculectomy. Every dB of additional VF loss at this stage is disproportionately functionally significant , the remaining field is the patient’s functional vision.
Steroid-responder: IOP rise following intravitreal, periocular, topical, or systemic steroids. Occurs in approximately 35-40% of patients with glaucoma or OHT. Switch to lower-IOP-effect steroid (fluorometholone, loteprednol) or add IOP-lowering drops. Significant IOP rise (above 35 mmHg): discontinue steroid if clinically possible.
Acute angle-closure crisis: Emergency. Pilocarpine 4% (constricts pupil, pulls iris from angle), IV acetazolamide 500 mg, topical beta-blocker and alpha-2 agonist, systemic hyperosmotic if needed. Laser peripheral iridotomy (LPI) once IOP is controlled.

Same-Day Assessment Required

Acute angle-closure attack: severe eye pain, headache, nausea/vomiting, haloes, dramatically reduced VA, red eye, fixed mid-dilated pupil, corneal edema, IOP commonly above 40-50 mmHg , requires emergency treatment
Neovascular glaucoma (rubeosis iridis): suspect in patients with DR, RVO, or ocular ischemic syndrome presenting with acute IOP rise and pain
Post-trabeculectomy: sudden pain, hypotony, very shallow AC, sudden VA decrease , suspect bleb leak, choroidal detachment, or aqueous misdirection

Acute angle-closure glaucoma causes IOP above 40 mmHg and is a true ocular emergency. IOP at this level damages the optic nerve within hours and causes corneal decompensation. The clinical triad of severe pain, haloes around lights, and reduced vision in a red eye with a fixed mid-dilated pupil should be recognized immediately in any clinical setting and referred to ophthalmology the same day. Primary care clinicians and emergency physicians need to know this presentation.

Clinical Pearls: Glaucoma

The LiGHT trial changed first-line glaucoma management. SLT is now a defensible first choice before drops.
LiGHT (Laser in Glaucoma and Ocular Hypertension, 2019) randomized 718 patients to SLT-first vs drops-first. At 36 months, 74% of SLT patients required no drops, disease control was equivalent between arms, and the SLT arm had better health economics. SLT is repeatable, avoids the adherence problem that makes drops less effective in the real world, and has minimal systemic side effects. It should be offered as an option to all suitable new POAG and OHT patients, not just reserved for drop failures.
A disc hemorrhage is a red flag. It often appears when IOP looks controlled.
Disc hemorrhages are frequently found at routine visits in patients whose IOP appears to be within target. They indicate active axonal damage at that moment, and predict measurable RNFL loss on subsequent OCT and VF deterioration. The error is to assume that because IOP is “normal for this patient” there is nothing to escalate. A disc hemorrhage warrants: reviewing whether the current target IOP is low enough, increasing visit frequency, and reconsidering whether progression is faster than tolerated. It is a signal the optic nerve sends , and it should be heard.
Adherence to glaucoma drops is worse than patients or clinicians assume. This matters more than drug choice.
Studies using electronic monitoring of drop bottles consistently show that patients take their glaucoma drops 50-70% of the time, compared with the near-100% reported in self-assessment. The most effective IOP-lowering drops are useless if not instilled. Simplifying regimens (once-daily PGA, fixed combinations), switching to SLT, and using preservative-free formulations to reduce discomfort are more likely to improve outcomes than switching between broadly equivalent second-line agents. Ask specifically about missed doses at every glaucoma review , without judgment.
Thin corneas lower measured IOP , and independently raise glaucoma risk.
GAT measures IOP by applanating the cornea , the thickness of the cornea affects the resistance to applanation and therefore the reading. Thin corneas (below 555 µm) cause GAT to underestimate true IOP. More clinically important: the OHTS trial demonstrated that thin CCT is an independent risk factor for conversion from OHT to POAG, separate from its effect on IOP measurement. A patient with “borderline” IOP of 22-23 mmHg and CCT of 520 µm is at higher risk than a patient with IOP of 26 mmHg and CCT of 600 µm. Measure CCT in all glaucoma and OHT patients.

Further reading: RCOphth Glaucoma Referral and Discharge Criteria and the AAO Preferred Practice Pattern , Primary Open-Angle Glaucoma. For shared-care context see the glaucoma subspecialty page and related conditions uveitis (uveitic glaucoma) and diabetic retinopathy (neovascular glaucoma).