Glaucoma Master Module · Lecture 2
Ocular Hypertension
Raised IOP without definite glaucoma
Raised IOP can be the first clue, but it is not by itself a diagnosis. This lecture shows how to establish ocular hypertension, assess the risk of future glaucoma, and choose between structured observation and preventive IOP lowering.
Clinical anchor
Ocular hypertension is a pressure-risk state, not glaucoma.
Core framework: [1–3,12]
Watch the Advanced Lecture
Before calculating risk or discussing treatment, confirm that the eye truly fulfils the definition of primary ocular hypertension.
Locked definition
Primary ocular hypertension is consistently elevated intraocular pressure in an eye with an open angle, no identifiable secondary cause of IOP elevation, and no definite glaucomatous structural or functional damage.
Not simply “IOP >21 mmHg”-
Repeatable IOP elevation
- Do not label OHT after one isolated IOP reading.
- Confirm the pressure pattern with repeat measurement.
- Interpret readings with timing, asymmetry, corneal context, medication influence, and disc–OCT–field correlation.
-
Open angle
- Establish angle status at the initial assessment.
- Gonioscopy directly visualises the angle and can reveal secondary clues.
- Van Herick estimates peripheral chamber depth; it does not replace gonioscopy.
-
No secondary cause
- Screen for steroid response, pseudoexfoliation, pigment dispersion, trauma, and inflammation.
- Consider lens-related mechanisms, raised episcleral venous pressure, and other causes suggested by the clinical picture.
-
No definite glaucomatous damage
- No convincing glaucomatous optic-disc or rim change.
- No convincing RNFL or macular ganglion-cell damage.
- No reliable and reproducible glaucomatous field defect.
- A normal field alone does not exclude glaucoma.
- Raised IOP alone does not equal ocular hypertension.
- Open angle alone does not prove primary OHT; secondary causes must still be excluded.
- OHT is a narrower phenotype within the broader POAG-suspect spectrum.
Sources: [1–3,12]
The conventional upper limit of 21 mmHg is useful for orientation, but it is not a biological cut-off between healthy eyes and glaucoma. [4,12]
Classical examination teaching
Where did 21 come from?- Mean IOP was historically described as around 16 mmHg.
- The conventional population range is around 11–21 mmHg.
- IOP was described as approximately bell-shaped, with a right-hand tail of higher values.
- The upper limit of 21 mmHg was derived from approximately two standard deviations above the mean.
Historical population teaching: [4,12]
Clinical interpretation
Think beyond one number.- IOP of 22 mmHg does not diagnose glaucoma.
- IOP of 18 mmHg does not exclude glaucoma.
- Pressure must be interpreted alongside the optic nerve, OCT, visual field, and overall clinical context.
Clinical interpretation: [1,2,12]
Raised IOP is a finding. It is not yet a diagnosis.
Kanski examination note
- Kanski’s Clinical Ophthalmology, 9th edition, gives a classical estimate of OHT in around 4–7% of people above 40 years.
- This refers to raised IOP, open angles, and no detectable glaucomatous damage.
- It is not a universal prevalence figure: prevalence varies with population, age, diagnostic definition, and method of IOP measurement.
Reference 12: Salmon JF. Kanski’s Clinical Ophthalmology: A Systematic Approach. 9th ed. Edinburgh: Elsevier; 2020. [12]
Sources: [1,2,4,12]
These terms can overlap clinically, but they are not interchangeable. Primary ocular hypertension is the narrow raised-pressure, no-definite-damage phenotype within the broader suspect spectrum. [1–3]
| Category | IOP | Angle | Damage status | Main action |
|---|---|---|---|---|
| Primary ocular hypertension | Elevated | Open | No definite glaucomatous damage | Risk-stratify; observe or consider preventive IOP lowering |
| POAG suspect | Normal or elevated | Open | Suspicious but not definite disc, OCT, or field findings | Investigate and monitor through the suspect pathway |
| Early glaucoma | Normal or elevated | Open | Definite structural and/or functional glaucomatous damage | Reclassify and manage as glaucoma |
| Secondary ocular hypertension | Usually elevated | Variable | Depends on the cause | Identify the cause; do not use the primary-OHT pathway |
| Angle-closure disease | May be elevated | Narrow, occludable, or closed | Variable | Redirect to the angle-closure pathway |
Ocular hypertension is not a static lifelong label. During follow-up, an eye may move to a glaucoma pathway when definite glaucomatous damage appears, or to another pathway when a secondary cause or angle abnormality is recognised. [1–3]
Sources: [1–3]
The baseline visit is not simply about recording raised IOP. It creates the reference point against which later change can be recognised. [1–3,5–7]
In ocular hypertension, baseline documentation is how future conversion becomes recognisable.
History and risk context
Ask what changes the picture.- Previous IOP values and duration of pressure elevation, if known.
- Family history and fellow-eye status.
- Steroid exposure, trauma, inflammation, previous surgery, and medication history.
- Ability to attend follow-up, access to testing or treatment, cost concerns, and adherence likelihood.
- Ocular surface disease and patient preferences before preventive treatment is considered.
Examination and investigations
Build a reliable starting record.- Repeat Goldmann IOP where possible.
- Gonioscopy and slit-lamp assessment for secondary clues.
- Central corneal thickness.
- Optic-disc examination with baseline disc photography where possible.
- OCT where appropriate and reliable standard automated perimetry.
Document uncertainty as well
- Record whether IOP, imaging, and visual-field tests are reliable.
- Do not treat an equivocal OCT colour code or doubtful field point as definite disease.
- Future interpretation depends on test quality, comparability, and longitudinal change.
Sources: [1–3,5–7]
Ocular hypertension does not carry the same risk in every eye. The OHTS–EGPS model uses five variables to estimate the five-year probability of developing early primary open-angle glaucoma. [6,7]
The model estimates risk. Clinical judgment decides what that risk means for the individual patient.
Age
- Older age increases the model-estimated five-year risk.
- Younger age gives fewer points in the model, but may still imply longer lifetime IOP exposure.
Mean untreated IOP
- Higher confirmed untreated IOP increases modelled risk.
- Interpret IOP as part of the full risk profile, not as a stand-alone diagnosis.
Mean CCT
- Thin central corneal thickness is associated with greater conversion risk.
- CCT also provides context for interpreting Goldmann IOP.
Vertical cup-to-disc ratio
- A larger vertical cup-to-disc ratio increases modelled risk.
- Disc size, rim configuration, OCT, field findings, and change over time still matter.
Pattern standard deviation (PSD)
- Higher PSD reflects greater localised irregularity in visual-field sensitivity and increases modelled risk.
- PSD alone does not diagnose glaucoma; interpret it with field reliability, pattern, repeatability, disc, OCT, and structure–function correlation.
Older age · Higher untreated IOP · Thin CCT · Larger vertical cup-to-disc ratio · Higher PSD
Keep the model in its place
- These variables estimate five-year conversion risk; they do not establish the diagnosis.
- Family history matters clinically, even though it is not one of the five formal calculator variables.
- A calculated risk supports decision-making; it does not replace clinical judgment.
Sources: [6,7,13,14]
CCT matters in two ways: it provides context for interpreting Goldmann IOP, and it contributes to the overall risk profile in ocular hypertension. [7,8]
Treat CCT as a measurement-context variable and a risk-context variable.
Measurement context
- Goldmann applanation is influenced by corneal thickness and corneal properties.
- A thinner cornea may require less force to flatten; a thicker cornea may require more force.
- Thickness alone cannot accurately calculate the individual measurement error.
Measurement context: [8,17]
Risk context
- Thin CCT was associated with greater conversion risk in the OHTS–EGPS prediction model.
- Thick CCT may be associated with lower modelled risk, but does not make the eye safe.
- CCT should be read alongside IOP, disc appearance, PSD, age, and wider clinical context.
Risk context: [7,8]
Traditional corrected IOP = measured IOP + 0.7 × (520 − CCT) ÷ 10
CCT is in micrometres. The traditional approximation is 0.7 mmHg for every 10 µm deviation from 520 µm. [17]
Examination shortcut — use it as an approximation.
Example 1 — Thin cornea
Thinner than 520? Traditionally add.- Measured IOP: 20 mmHg
- CCT: 500 µm
- 500 µm is 20 µm thinner than 520 µm.
- → Traditional addition = 1.4 mmHg
21.4 mmHg
Example 2 — Thick cornea
Thicker than 520? Traditionally subtract.- Measured IOP: 20 mmHg
- CCT: 540 µm
- 540 µm is 20 µm thicker than 520 µm.
- → Traditional subtraction = 1.4 mmHg
18.6 mmHg
Clinical correction
- Do not describe the calculated value as the patient’s exact “true IOP.”
- Different correction formulas give different values, and corneal biomechanics are not captured by thickness alone.
- CCT-based correction formulas did not improve POAG prediction in OHTS analysis.
Clinical safeguard: [8,17]
Sources: [7,8,17]
In the selected OHTS population, topical IOP lowering reduced the five-year cumulative incidence of primary open-angle glaucoma. [5]
The likely benefit of immediate treatment depends on the patient’s baseline risk.
Five-year cumulative incidence of POAG
9.5%
Developed POAG over five years.
4.4%
Developed POAG over five years.
OHTS primary treatment result: [5]
Lower-risk patients may gain little absolute benefit from immediate treatment. Higher-risk patients may gain more from earlier IOP lowering.
OHTS treatment target
- At least 20% IOP reduction.
- IOP of 24 mmHg or lower.
What not to conclude
- These were OHTS protocol targets.
- They are not universal targets for every patient with OHT.
Keep the evidence in context
- OHTS studied a selected cohort aged 40–80 years with open angles, normal discs, and normal reliable fields at entry.
- OHTS studied topical medication; it did not establish one universal present-day first-line modality for all OHT.
- Long-term data are not pure untreated natural history because treatment status changed over time.
Sources: [5,6,9,10]
EGPS means European Glaucoma Prevention Study. Together with OHTS data, the model combines the five formal variables discussed above to estimate a patient’s five-year probability of developing early POAG. [6,7]
Use a numerical estimate to structure discussion, not to replace clinical judgment.
A 10% five-year risk means that among 100 patients with a similar profile, around 10 may develop early POAG over five years. It does not mean that an individual patient will definitely convert.
Probability, not certainty.What the model estimates
- Five-year probability of developing early POAG.
- Relative impact of the five formal OHTS–EGPS variables in combination.
- A numerical estimate that can support counselling and risk discussion.
Model purpose: [6,7]
What it does not estimate
- Certainty of conversion in one individual patient.
- Lifetime visual disability or progression after established glaucoma.
- Adherence, need for surgery, or risk from a secondary glaucoma mechanism.
Model limits: [7,13,14]
When does the calculator add value?
Most useful when
- The diagnosis is secure and the patient resembles the OHTS–EGPS context.
- The observe-versus-treat decision is not obvious.
- Several variables are mildly unfavourable and a numerical estimate improves counselling.
Adds less when
- The profile is clearly low risk or clearly treatment-leaning.
- The eye has definite glaucoma, a secondary cause, or narrow/occludable angles.
- Field reliability or diagnostic certainty is poor.
Practical applicability: [7,13,14]
Use extra caution outside the original study context
Be cautious when age is below 30 or above 80 years, untreated IOP is below 20 or above 32 mmHg, CCT is below 475 or above 650 µm, or the diagnosis and testing are uncertain. A calculator cannot rescue an uncertain diagnosis. [7,13,14]
Sources: [6,7,13,14]
A five-year estimate is useful, but treatment decisions should consider whether that risk is likely to matter over the patient’s remaining lifetime. [7,9,10]
The calculator quantifies short-term risk; the clinician interprets its relevance for the individual patient.
| Risk group | Five-year risk | General interpretation |
|---|---|---|
| Low risk | <6% | Immediate treatment produced little absolute benefit in delayed-treatment analysis when surveillance was reliable. |
| Intermediate risk | 6–13% | Interpret the full variable pattern, expected duration of exposure, and patient context before deciding between observation and preventive lowering. |
| High risk | >13% | Earlier IOP lowering is more likely to offer meaningful absolute benefit. |
Delayed-treatment risk grouping: [9,10]
Lifetime exposure
- Older age increases the model-estimated short-term risk.
- Younger age may produce a lower five-year estimate but implies a longer period of potential IOP exposure.
- A lower short-term score should not automatically make a young patient clinically unimportant.
Treatment-leaning signals
- Several unfavourable variables clustering together increase concern.
- An untreated IOP around 30 mmHg is a strong treatment-leaning signal, not a one-number mandate.
- Confirm the diagnosis and interpret pressure in the full clinical context before acting.
A discordant profile is possible: a patient may have a modest calculated risk but a long anticipated exposure period, or a treatment-leaning IOP with uncertainty that still needs clarification. Risk calculation structures judgment; it does not replace it.
Sources: [1,2,7,9,10]
Management begins only after the diagnostic boundary is secure. The decision combines five-year risk, lifetime context, and the practical burden of care. [1–3,7]
The relevant question is whether the patient has sufficient risk of visual impairment during their lifetime for preventive lowering to be worthwhile.
| Pathway | When it may fit | What it requires |
|---|---|---|
| Active observation | Secure primary OHT, lower meaningful risk, reliable baseline testing, and a patient able to attend surveillance. | A documented follow-up plan with IOP, disc, OCT, and field review according to the clinical question. |
| Preventive IOP lowering | Higher-risk variables cluster, lifetime exposure is meaningful, IOP is markedly raised, follow-up is less reliable, or patient preference favours risk reduction. | Shared decision-making about the likely benefit, treatment burden, suitability, and surveillance after treatment begins. |
| Reclassify or redirect | Secondary cause, narrow or occludable angle, definite glaucomatous damage, or unresolved diagnostic uncertainty. | Leave the primary-OHT pathway and manage the relevant diagnosis or complete clarification first. |
Management framework: [1–3,7]
Age 61 years, untreated IOP 29 mmHg, CCT 520 µm, vertical CDR 0.55, and PSD 2.6 dB gives a simplified score of 16 and an estimated five-year risk of ≥33%. This is treatment-leaning, but still not an automatic treatment order.
High calculated risk still needs clinical context.NICE: a pathway example, not a universal threshold
NICE approach for newly diagnosed OHT
- Assess future risk of visual impairment using IOP, CCT, family history, life expectancy, and other relevant factors.
- For IOP ≥24 mmHg with meaningful lifetime visual risk, offer 360° SLT when suitable.
- Use a generic prostaglandin analogue when SLT is unsuitable, declined, delayed, or insufficient.
Do not overread the number
- This is a UK guideline pathway, not a biological rule that every IOP of 24 mmHg requires treatment.
- SLT versus topical treatment depends on suitability, angle status, ocular surface disease, adherence, cost, access, contraindications, and preference.
NICE and SLT context: [3,11]
A risk estimate informs the conversation. Diagnostic certainty, expected lifetime exposure, treatment burden, and patient circumstances determine the final plan.
Sources: [1–3,7,11]
The simplified score assigns points to the five formal OHTS–EGPS variables. Add the five scores, then map the total to an estimated five-year risk of early POAG. [7]
A point total organises multivariable risk. It does not decide treatment on its own.
| Variable | 0 points | 1 point | 2 points | 3 points | 4 points |
|---|---|---|---|---|---|
| Age | <45 years | 45–<55 years | 55–<65 years | 65–<75 years | ≥75 years |
| Mean untreated IOP | <22 mmHg | 22–<24 mmHg | 24–<26 mmHg | 26–<28 mmHg | ≥28 mmHg |
| Mean CCT | >600 µm | 576–600 µm | 551–575 µm | 526–550 µm | ≤525 µm |
| Mean vertical CDR | <0.3 | 0.3–<0.4 | 0.4–<0.5 | 0.5–<0.6 | ≥0.6 |
| Mean PSD | <1.8 dB | 1.8–<2.0 dB | 2.0–<2.4 dB | 2.4–<2.8 dB | ≥2.8 dB |
Simplified OHTS point system: [7]
Step 2 — Convert the total into five-year risk
The total score is linked to the following approximate five-year probability of early POAG.
Important safeguards
- This is a teaching simplification; a continuous calculator may generate a different estimate.
- Use the score only after the diagnosis is secure and secondary or angle-closure mechanisms have been excluded.
- Risk calculation supports judgment; it is not an automatic treatment mandate.
Sources: [7]
Surveillance is how a pressure-risk state is monitored for change into definite disease. The interval should reflect both risk and diagnostic uncertainty. [3]
Test frequency follows the clinical question.
| Clinical context | Typical interval | Why earlier or later review may be needed |
|---|---|---|
| Low-risk untreated OHT with secure diagnosis and reliable follow-up | ~12 months | Longer surveillance is reasonable only when the baseline is secure and attendance is reliable. |
| Intermediate-risk or mixed-variable profile | 6–12 months | Individualise according to IOP level, risk pattern, anticipated lifetime exposure, and reliability of prior tests. |
| Uncertain IOP, disc, OCT, or visual-field finding | Earlier — within months | Clarify whether an apparent abnormality is noise, artefact, or definite disease. |
| New treatment or uncontrolled IOP | 1–4 months | Assess response, adverse effects, adherence, and whether the chosen plan is working. |
| Treated and controlled, but conversion remains uncertain | 6–12 months | Continue targeted structural and functional surveillance. |
| Treated and controlled, with no evidence of conversion | 18–24 months | NICE provides specific treated-OHT review bands; apply them in the relevant guideline context. |
Surveillance intervals and NICE context: [3]
Usually review
- IOP trend rather than a single isolated value.
- Anterior segment and slit-lamp findings where clinically relevant.
- Optic nerve appearance and documentation over time.
- Adherence and adverse effects when treatment has begun.
Add targeted testing when needed
- Repeat visual field, OCT, or disc photographs when surveillance or a new concern requires comparison.
- Repeat gonioscopy when angle status or the clinical context indicates it.
- Interpret every test with its quality, reproducibility, and relevance to the clinical question.
A normal result at one visit does not end surveillance. Longitudinal comparison is what distinguishes stable risk from emerging disease.
CCT is usually a baseline measurement
Repeat CCT is not routinely needed at every visit unless the cornea or the clinical context has changed.
Sources: [3]
Follow-up is not just about confirming that IOP remains elevated. The central question is whether there is now definite glaucomatous structural or functional damage. [1–3]
Ocular hypertension is not a static lifelong category. During surveillance, the eye may remain stable or be reclassified as definite glaucoma.
Has this patient moved from a pressure-risk state to definite glaucomatous disease?
Evidence that supports conversion
- Progressive focal rim thinning or a new anatomically plausible notch.
- Progressive, high-quality, comparable OCT change consistent with glaucoma.
- Repeatable visual-field loss with a compatible glaucomatous pattern.
- Structure–function agreement and longitudinal progression where available.
Evidence of conversion: [1–3,18]
What IOP contributes
- IOP trend remains important for risk assessment and treatment response.
- Higher IOP alone does not prove that glaucoma has developed.
- A stable IOP does not exclude structural or functional conversion.
- IOP must be interpreted alongside the disc, OCT, field, and time course.
IOP in longitudinal interpretation: [1–3]
| Finding | Before labelling glaucoma | What would increase confidence? |
|---|---|---|
| New OCT abnormality | Check scan quality, segmentation, signal, artefact, and anatomical plausibility. | Comparable repeat imaging, focal progression, disc correlation, and compatible functional change. |
| New visual-field defect | Check reliability, learning effect, pattern consistency, and whether it is repeatable. | A reproducible glaucomatous defect with structural correlation. |
| Suspicious disc appearance | Compare photographs, disc size, rim configuration, asymmetry, and baseline documentation. | Definite progressive rim loss or a new plausible focal notch over time. |
Test-quality and longitudinal safeguards: [1–3,18]
Read change in context
- There is no single universal RNFL-loss rate that independently proves conversion.
- Concern rises when change is focal, progressive, high quality, comparable, and anatomically plausible.
- Disc findings and visual-field correlation strengthen the meaning of a possible OCT trend.
The calculator helps decide what to do with risk. Serial examination determines whether risk has become disease.
Sources: [1–3,18]
This case shows how a patient can be appropriately classified as primary ocular hypertension at baseline and later be reclassified when definite disease appears. [1–3,7]
55-year-old patient
Repeated IOP 24–25 mmHg OU
Primary OHT at baseline → later right-eye conversion
Follow-up is not about defending the initial label. It is about recognising when the patient’s clinical category has changed.
Is this primary ocular hypertension?
The initial work-up confirms pressure elevation but finds no definite glaucomatous structural or functional damage.
| Clinical domain | Baseline findings | Meaning at baseline |
|---|---|---|
| Pressure profile | Repeated IOP 24–25 mmHg in both eyes. | IOP elevation is confirmed and requires diagnostic assessment plus risk stratification. |
| Angle and cause | Open angles; no pseudoexfoliation, pigment dispersion, steroid exposure, trauma, or inflammation. | Primary-OHT pathway remains appropriate. |
| Cornea | CCT 610 µm. | CCT is part of measurement and risk context; it does not make the eye “safe.” |
| Disc, OCT, and field | Healthy discs with vertical CDR 0.3; no glaucomatous OCT abnormality; reliable visual fields with PSD 1.6 dB. | No definite structural or functional glaucomatous damage. |
The eye fulfils the definition of primary ocular hypertension. Structured observation is reasonable because the diagnosis is secure, the baseline is reliable, and there is no definite glaucoma.
2 + 2 + 0 + 1 + 0 = 5 points
≤4% estimated five-year risk
Primary OHT, reliable baseline, low estimated five-year risk.
Structured observation with longitudinal comparison.
New concordant findings in the right eye require reclassification.
What has changed?
The relevant new findings are in the right eye. This teaching case is illustrating unilateral reclassification rather than claiming bilateral progression.
| Follow-up domain | New right-eye finding | Why it matters |
|---|---|---|
| IOP trend | IOP is now higher in the right eye. | Higher IOP adds concern but does not, by itself, prove glaucoma. |
| Optic nerve and OCT | New focal inferior rim thinning with a new corresponding inferior RNFL abnormality. | There is new, anatomically plausible structural change compared with baseline. |
| Visual field | A matching superior visual-field defect is reliable and repeatable. | There is compatible functional change that agrees with the structural pattern. |
The right eye should now be reclassified and managed as glaucoma, because progressive structural change is supported by a matching reliable, repeatable functional defect.
Later conversion does not prove that the original diagnosis or decision to observe was wrong. It demonstrates the value of reliable baseline records and structured surveillance.
Sources: [1–3,7,18]
Keep the diagnosis, risk estimate, and surveillance plan separate. [1–3,7,8]
A raised pressure, a risk score, or one abnormal test is not enough on its own.
| Do not confuse | Remember |
|---|---|
| IOP >21 mmHg with glaucoma | Twenty-one mmHg is a statistical convention. Raised IOP is a finding, not a diagnosis. |
| IOP ≤21 mmHg with absence of glaucoma | Glaucoma can occur at lower measured IOP values. |
| One raised reading with established OHT | Confirm the pressure profile and assess the angle, cause, disc, OCT, and field. |
| Open angle with primary OHT | Exclude secondary causes before using the primary-OHT pathway. |
| Thin CCT with exact “true IOP” | Historical correction formulas are approximations; CCT is measurement and risk context, not a precise correction. |
| Thick CCT with a “safe” eye | Thick cornea may lower estimated risk, but does not remove the need for surveillance. |
| Normal field or one abnormal OCT/VF result with a final diagnosis | Interpret structure, function, quality, repeatability, and time together. |
| Risk score with an automatic treatment decision | The score structures judgment; diagnostic certainty, lifetime context, and patient factors determine the plan. |
| Low risk with discharge | Observation is active care with a documented follow-up plan. |
Diagnostic, CCT, and risk-calculation safeguards: [1–3,7,8]
OHT is a pressure-risk state, not glaucoma. The goal is secure diagnosis, proportionate prevention, and structured surveillance.
Sources: [1–3,7,8]
Approach ocular hypertension in a fixed sequence: establish the diagnosis, estimate risk, consider lifetime context, and monitor for definite disease.
Confirm the OHT phenotype.
Repeatably elevated IOP, an open angle, no identifiable secondary cause, and no definite glaucomatous structural or functional damage.
Do not diagnose from “21 mmHg.”
It is a historical statistical convention. Raised IOP is a finding, not glaucoma by itself.
Read the profile, not one variable.
Age, untreated IOP, CCT, vertical CDR, and PSD provide a five-year estimate of early POAG risk; they do not independently establish disease.
Observe, lower IOP preventively, or reclassify.
The plan depends on diagnostic certainty, calculated risk, expected lifetime exposure, follow-up reliability, treatment burden, and patient context.
Look for longitudinal conversion.
Serial disc examination, OCT, and visual fields determine whether risk has become definite glaucomatous disease.
Ocular hypertension is a pressure-risk state, not glaucoma. Good care means proportionate prevention and structured surveillance—not automatic treatment or automatic reassurance.
Sources: [1–3,5–10]
Evidence base cited throughout this ocular hypertension lecture.
Pazos M, Traverso CE, Viswanathan A, et al; European Glaucoma Society. European Glaucoma Society – Terminology and guidelines for glaucoma, 6th Edition. Br J Ophthalmol. 2025;109(Suppl 1):1-212. doi:10.1136/bjophthalmol-2025-egsguidelines.
Gedde SJ, Kolomeyer NN, Challa P, Chopra V, Vinod K, Bowden EC, Budenz DL; American Academy of Ophthalmology Preferred Practice Pattern Glaucoma Committee. Primary Open-Angle Glaucoma Suspect Preferred Practice Pattern®. Ophthalmology. 2026;133(4):P104-P152. doi:10.1016/j.ophtha.2025.12.028.
National Institute for Health and Care Excellence. Glaucoma: diagnosis and management. NICE guideline NG81. London: NICE; 2017. Updated 2022 Jan 26.
Hollows FC, Graham PA. Intra-ocular pressure, glaucoma, and glaucoma suspects in a defined population. Br J Ophthalmol. 1966;50(10):570-586. doi:10.1136/bjo.50.10.570.
Kass MA, Heuer DK, Higginbotham EJ, et al; Ocular Hypertension Treatment Study Group. The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002;120(6):701-713. doi:10.1001/archopht.120.6.701.
Gordon MO, Beiser JA, Brandt JD, et al; Ocular Hypertension Treatment Study Group. The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002;120(6):714-720. doi:10.1001/archopht.120.6.714.
Gordon MO, Torri V, Miglior S, et al; Ocular Hypertension Treatment Study Group; European Glaucoma Prevention Study Group. Validated prediction model for the development of primary open-angle glaucoma in individuals with ocular hypertension. Ophthalmology. 2007;114(1):10-19. doi:10.1016/j.ophtha.2006.08.031.
Brandt JD, Gordon MO, Gao F, Beiser JA, Miller JP, Kass MA. Adjusting intraocular pressure for central corneal thickness does not improve prediction models for primary open-angle glaucoma. Ophthalmology. 2012;119(3):437-442. doi:10.1016/j.ophtha.2011.03.018.
Kass MA, Gordon MO, Gao F, et al; Ocular Hypertension Treatment Study Group. Delaying treatment of ocular hypertension: the Ocular Hypertension Treatment Study. Arch Ophthalmol. 2010;128(3):276-287. doi:10.1001/archophthalmol.2010.20.
Kass MA, Heuer DK, Higginbotham EJ, et al; Ocular Hypertension Study Group. Assessment of cumulative incidence and severity of primary open-angle glaucoma among participants in the Ocular Hypertension Treatment Study after 20 years of follow-up. JAMA Ophthalmol. 2021;139(5):558-566. doi:10.1001/jamaophthalmol.2021.0341.
Gazzard G, Konstantakopoulou E, Garway-Heath D, et al; LiGHT Trial Study Group. Selective laser trabeculoplasty versus eye drops for first-line treatment of ocular hypertension and glaucoma: a multicentre randomised controlled trial. Lancet. 2019;393(10180):1505-1516. doi:10.1016/S0140-6736(18)32213-X.
Salmon JF. Kanski’s Clinical Ophthalmology: A Systematic Approach. 9th ed. Edinburgh: Elsevier; 2020.
Wright D, Wu H, King A, Montesano G, Higgins B, Gazzard G, et al. Validating and updating the OHTS-EGPS model predicting 5-year glaucoma risk among patients with ocular hypertension using electronic medical records: a cohort study. Health Technol Assess. 2026;30(25):1-35. doi:10.3310/GJAA0514.
Boland MV, Quigley HA, Lehmann HP. The impact of risk calculation on treatment recommendations made by glaucoma specialists in cases of ocular hypertension. J Glaucoma. 2008;17(8):631-638. doi:10.1097/IJG.0b013e3181659e6a.
Tran VT. UBM/slit-lamp-photo imaging of pseudoexfoliation deposits in the iridocorneal angle: imaging clues to the genesis of ocular hypertension. Int Ophthalmol. 2009;29(5):389-392. doi:10.1007/s10792-008-9254-y.
Sit AJ, Nau CB, McLaren JW, Johnson DH, Hodge D. Circadian variation of aqueous dynamics in young healthy adults. Invest Ophthalmol Vis Sci. 2008;49(4):1473-1479. doi:10.1167/iovs.07-1139.
Ehlers N, Bramsen T, Sperling S. Applanation tonometry and central corneal thickness. Acta Ophthalmol (Copenh). 1975;53(1):34-43. doi:10.1111/j.1755-3768.1975.tb01135.x.
Jeong D, Sung KR, Jo YH, Yun SC. Age-related physiologic thinning rate of the retinal nerve fiber layer in different levels of myopia. J Ophthalmol. 2020;2020:1873581. doi:10.1155/2020/1873581.
Yang Y, Zhang X, Chen Z, Wei Y, Ye Q, Fan Y, et al; LiGHT China Trial Study Group. Intraocular pressure and diurnal fluctuation of open-angle glaucoma and ocular hypertension: a baseline report from the LiGHT China trial cohort. Br J Ophthalmol. 2023;107(6):823-827. doi:10.1136/bjophthalmol-2021-320128.
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