Glaucoma

1. The problem, which is that you cannot feel it

Glaucoma is progressive damage to the optic nerve, and it is the leading cause of irreversible blindness worldwide. That word is the whole reason this chapter exists: sight lost to glaucoma does not come back. Everything useful happens before it is lost.

2. Eye pressure, and what the numbers actually mean

The eye continuously makes a clear fluid called aqueous humour and continuously drains it, mostly through a sieve-like structure at the angle where the iris meets the cornea. Pressure is what you get when production and drainage are not in balance — almost always because drainage has become inefficient, not because the eye is making too much.

And a single reading is a poor measurement. Pressure varies through the day — often by several mmHg, typically highest in the morning — and it varies with posture, exertion, caffeine and how tightly you are squeezing your eyelids against the tonometer. A number taken once at 3pm is one sample from a moving quantity.

3. Why a high number often means nothing at all

This is the part that causes the most unnecessary alarm, and it is settled by a large trial.

But the average conceals an enormous spread, and that is the useful finding. When the same trial stratified people by their other characteristics, the five-year risk ran from about 1–2% in the lowest-risk group to 25–35% in the highest. Same label, same “ocular hypertension” on the notes, and something like a twentyfold difference in what happens next.

What separated them:

• Age — older is higher risk
• How high the pressure actually is — 22 and 32 are not the same problem
• A thinner cornea — one of the strongest predictors in the whole analysis
• A larger cup-to-disc ratio — how hollowed-out the optic disc already looks
• Higher pattern standard deviation on the visual field — a subtle irregularity in a field still classed as normal

And the mirror image is just as important. Normal-tension glaucoma is real and not rare: unmistakable optic nerve damage with pressures that never leave the normal range. A pressure of 16 does not exclude glaucoma, and this is precisely why the diagnosis rests on the nerve rather than the number.

4. What actually detects damage — the imaging

If pressure is the risk factor, imaging is the outcome. This is the part of the eye test that answers the question people think the pressure puff is answering.

Which is why baseline matters more than any single result. Nerve fibre layer thins with age in everyone. What identifies glaucoma is thinning faster than expected, in the pattern glaucoma makes, and you cannot see a rate from one visit. The first scan is mostly valuable for the scan five years later.

5. How fast it moves, and what decides that

The single most common fear on being diagnosed is going blind. For most people that is not what happens, and the reason is arithmetic.

• Most treated glaucoma progresses slowly enough never to cost useful sight in a normal lifetime. The disease is measured in decades.
• A minority progress fast, and identifying that minority early is essentially what glaucoma monitoring is for. Rates of visual field loss vary by more than an order of magnitude between people, which is why nobody can tell you your trajectory at diagnosis — only after several visits.
• The exceptions are specific, and they are the argument for the rest of this chapter: late diagnosis, when a large share of the field has already gone before anyone looked, and stopping treatment. Long-term series put blindness in one eye at roughly 10–15% at twenty years and bilateral blindness in the low single figures — low, and not zero, and concentrated in those two groups.
• Age at diagnosis is half the equation. Slow progression from 72 is very different from the same rate from 45. The clinical question is never just “is it progressing” but “is it progressing fast enough to matter given how long this person needs their eyes to last”, and that is why a younger patient is often treated more aggressively on identical numbers.

What is associated with faster progression:

• Higher untreated pressure, and less reduction achieved by treatment
• Pseudoexfoliation syndrome — flaky material in the eye, common in northern Europe, and one of the more aggressive forms
• A disc haemorrhage seen at the optic nerve head — a small bleed that is easy to miss and a recognised marker of ongoing damage
• Thin corneas, again
• Advanced damage already present at diagnosis
• Not taking the treatment, which is the commonest reason of all

6. How often to be tested

There is no single schedule, and anyone who gives you one without knowing your risk is guessing. The pattern in UK practice:

• No risk factors, no findings — a routine sight test roughly every two years, which is the standard NHS interval, and it is the interval at which glaucoma is most often first spotted.
• Over 40 with a first-degree relative who has glaucoma — annually, and your test is free in England on exactly that basis. Note what this is: an NHS entitlement designed around the group, not an NG81 monitoring schedule. NG81's intervals apply to people already under specialist care; this is the interval the free test is offered at, and it is the group that most reliably under-uses it.
• Ocular hypertension being monitored — typically somewhere between six months and two years, set by how the risk stratifies in section 3.
• Newly diagnosed or recently changed treatment — more often at first, because the priority is establishing a rate, and rates need several data points. Expect frequent visits early and fewer later; that is the plan working, not a scare.
• Stable, treated, long-standing — typically annually, sometimes longer.

NICE NG81 sets the monitoring intervals used in the NHS, and they depend on both the pressure and the state of the nerve. The useful question at an appointment is not when should I come back but “what is my rate of change, and what would make you bring me back sooner?”

7. The UK detection route, and the entitlements people do not claim

There is no national screening programme for glaucoma. Detection is opportunistic and happens almost entirely at a routine sight test — so the practical intervention is booking one.

NHS sight tests are free to more people than realise it. The rules differ across the four nations and are worth checking for where you live, but as a guide: everyone in Scotland; anyone aged 60 or over in England; and — the one most often missed — anyone aged 40 or over who has a parent, brother, sister or child diagnosed with glaucoma.

What a glaucoma-relevant test includes: pressure, a look at the optic disc, and a visual field check. Increasingly OCT as well, which many high-street practices now have. If you are over 40, have a family history, or are of Black African or Caribbean family origin — a group in whom glaucoma is both commoner and tends to present earlier — it is reasonable to ask whether all of those were done, and to ask for a copy of the OCT so the next person has a baseline.

8. Treatment in the UK, in order

The pathway changed in 2022 and most published advice has not caught up.

• Selective laser trabeculoplasty (SLT) — first-line. An outpatient laser, a few minutes, no incision. Works for most but not all, wears off over years, and is repeatable. Removes the daily-adherence problem entirely for the people it suits. Graded Strong as a first-line option — and not as superior to drops for preserving sight, because LiGHT's primary outcome was quality of life rather than visual field. You will meet the claim that SLT protects sight better, and there is something behind it — the six-year extension reported fewer eyes progressing in the SLT-first arm, roughly 20% against 27%, and fewer glaucoma operations. Those are secondary outcomes, so the honest position is that a signal exists and has not been tested as a primary endpoint, rather than that there is none.
• Prostaglandin analogue drops — latanoprost and relatives. Usually the first drug, once nightly, the most effective single class. Side effects are cosmetic and real: darker iris, longer lashes, hollowing of the eyelid skin.
• Beta blocker drops — timolol and relatives. Cheap and effective, and they are absorbed systemically: they can slow the heart and worsen asthma, so they are avoided in both. Pressing on the inner corner of the eye for a minute after a drop reduces that substantially, and almost nobody is told to.
• Carbonic anhydrase inhibitor and alpha agonist drops, and fixed combinations — added when one is not enough.
• Rho kinase inhibitors — and these are available here. Netarsudil (Rhokiinsa) has held a UK marketing authorisation since November 2019, and the latanoprost–netarsudil combination (Roclanda) is recommended by NICE under TA1009 for adults with open-angle glaucoma or ocular hypertension who have already been treated. A genuinely new mechanism — it acts on the drainage meshwork itself rather than on fluid production or the alternative outflow route. Whether a given clinic uses it is the specialist's call, but it is not, as American coverage sometimes implies and as an earlier version of this page wrongly said, unavailable in Britain.
• Preservative-free versions — benzalkonium chloride, the usual preservative, causes surface irritation and dry eye in a meaningful minority. If drops sting enough that you skip them, that is a reason to ask, not a reason to stop.
• Minimally invasive glaucoma surgery (MIGS) — small stents and devices, often done at the same time as cataract surgery, which is a genuinely efficient combination if you need both.
• Trabeculectomy — the long-established operation, creating a new drainage route. More effective and more demanding, with real complications and a lifetime of follow-up.
• Tube shunts and cyclodiode laser — for difficult or advanced disease.

9. Approved in the United States, not available here

A great deal of glaucoma coverage online is American, and the products below are described in it as though anyone could ask for them. They cannot, in the UK, at the time of writing. They are here so a reader recognises what they are reading rather than asking for something that does not exist here.

• Durysta (bimatoprost implant) — FDA approved March 2020. A biodegradable pellet placed in the front of the eye, releasing a prostaglandin for months. Approved for a single administration only, because repeat dosing caused corneal endothelial cell loss — about 3.5% at 18 months — and roughly 27% of trial patients had eye redness.
• iDose TR (travoprost implant) — FDA approved December 2023. A tiny titanium device anchored inside the eye giving continuous drug delivery for years. Phase 3 across 1,150 patients showed pressure reductions of 6.6–8.4 mmHg. The FDA has since permitted re-administration in patients with healthy corneas.
• Latanoprostene bunod — a prostaglandin that also donates nitric oxide, approved in the US.

Why the implants matter more than they sound. The single biggest failure in glaucoma care is not that treatments are weak — it is that drops do not get put in. A treatment that works for three years without the patient doing anything removes the largest practical problem in the disease. That is the direction the whole field is moving, and it is why this list is worth watching even from a country where none of it is available yet.

10. What is coming

• Longer and repeatable implants. A next-generation iDose with roughly double the drug capacity is in phase IIb/III. A biodegradable latanoprost implant has reported 26–35% pressure reduction sustained over 48 weeks with 94% of participants needing no drops at all — and, unlike Durysta, no signal of corneal endothelial harm on repeat dosing, which is the thing that would make implants routine rather than exceptional.
• Drug-eluting contact lenses and punctal plugs — a bimatoprost-loaded printed lens has matched daily drops in phase IIb.
• Drug-delivering intraocular lenses — medication built into the lens implanted during cataract surgery, so one operation treats two conditions.
• AI progression detection. Probably the nearest-term change of all, and the one most likely to reach the UK first: automated detection of change across OCT scans, fundus photos and visual fields. The regulatory path is already established through diabetic retinopathy screening. Its value is precisely the problem in section 5 — spotting rate of change earlier than a human comparing images by eye.
• Neuroprotection — protecting the nerve rather than lowering pressure. Covered in full, with the specialty societies' position on it, in what is being sold for glaucoma. The phase 3 answer arrives in late 2027.

Availability checked August 2026. This section will age faster than anything else in this topic. Treat it as a description of the direction of travel rather than as a current formulary.

11. The one form that is an emergency

12. What actually reduces your risk

There is no lifestyle change with good evidence for preventing glaucoma, and this page will not invent one. What there is, in order of how much it is worth:

• Get tested, and get your relatives tested. Early detection is the only intervention here with a large effect, and family history is the flag that should trigger it. If you have glaucoma, your siblings and children need to know the number 40 and the word “free”.
• If you are diagnosed, use the treatment. Non-adherence is the commonest reason glaucoma progresses in someone already under care, and it is rarely carelessness — drops sting, they are fiddly, and the disease gives you no feedback for missing them. Say so, and ask for a laser, a preservative-free version, or a different class.
• Do not stop because your vision seems fine. It will seem fine until it is not, and the part that has gone does not return.
• Ask for your corneal thickness, once. It reinterprets every pressure reading you will ever have, takes seconds, and never needs repeating.
• Ask what your rate of change is, rather than what your pressure was today. Rate is the thing that decides your outcome, and it is the thing patients are least often told.
• Keep a copy of your scans. Baseline imaging is worth most to whoever sees you in ten years, and records move badly between practices.
• Smoking and cardiovascular health plausibly matter through ocular blood flow. The evidence is weaker than for the eye conditions in the macular degeneration chapter, and both are worth doing for reasons that are far better evidenced.

And the thing this chapter would most like you to take from it: if you are over 40 and have a parent or sibling with glaucoma, your sight test is probably free and you have probably not booked one.