Ocular Hypertension
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Summary
Ocular Hypertension (OHTN), as defined by the Ocular Hypertension Treatment Study (OHTS), is a risk state characterized by elevated intraocular pressure (IOP) without optic nerve damage or visual field loss, distinguishing it from primary open-angle glaucoma (POAG), which requires reproducible structural and/or functional glaucomatous damage. In OHTS, patients aged 40–80 with open angles, normal optic discs, and normal visual fields but IOPs of 24–32 mm Hg were followed longitudinally. The study demonstrated that many patients with OHTN do not progress to glaucoma, underscoring that elevated IOP alone is insufficient for a POAG diagnosis or for automatic treatment. The European Glaucoma Prevention Study (EGPS), similarly demonstrated heterogeneity in progression risk among individuals with ocular hypertension, reinforcing the concept that OHTN is a variable risk condition rather than an obligate precursor to glaucoma.
Key predictors of conversion to POAG, include thin central corneal thickness (CCT < 555), higher baseline IOP (>24), larger vertical cup-to-disc ratio, and older age. Pooled analysis of OHTS and the EGPS showed that central corneal thickness is one of the strongest risk factors, influencing both true IOP estimation and intrinsic optic nerve susceptibility to damage. Importantly, structural optic nerve changes often preceded detectable visual field loss, reinforcing the value of careful optic nerve assessment in at-risk patients. A notable limitation of both stduies is that optical coherance tomography of the retinal nerve fiber layer (OCT RNFL) was not available, potentially leading to underdetection of early glaucomatous damage.
Clinically, OHTS demonstrated that IOP lowering with topical ocular hypotensive medications reduces the risk of developing POAG by approximately 60% over five years, with treated patients showing a 4.4% incidence is developing POAG versus 9.5% incidence of developing POAG in untreated patients. Long-term follow-up demonstrated that high-risk patients derive the greatest absolute benefit from early treatment, while low-risk individuals have a very low likelihood of progression even over decades and can be safely observed. The central clinical takeaway is that management of OHTN should be individualized using risk stratification rather than IOP alone, balancing the modest absolute risk reduction against lifelong treatment burden.
Disease Entity
Disease
Ocular hypertension is a common clinical entity defined as intraocular pressure (IOP) consistently greater than 21 mmHg without evidence of optic nerve damage, retinal nerve fiber layer loss, or visual field defects on standard testing. It is highly relevant to practicing ophthalmologists as it represents the strongest modifiable risk factor for progression to primary open-angle glaucoma (POAG).[1] OHTN excludes secondary causes of elevated IOP, including steroid response, pigment dispersion, pseudoexfoliation, inflammation, or trauma.
Risk Factors
Risk factors of developing glaucoma include:
- thin corneas (CCT<555)
- large vertical cup-to-disc ratio
- african american race
- positive family history
- older age
- myopia, hypertension, diabetes, corticosteroid use
The strongest predictors are thin corneas, higher IOPs, and larger vertical cup-to-disc ratio.[1][2]
Pathophysiology
Aqueous humor predominantly flows out of the anterior chamber via 2 pathways: the trabecular meshwork and the uveoscleral pathway. The trabecular pathway involves aqueous humor flowhrough the trabecular meshwork and into Schlemm's canal. The uveoscleral pathway involves aqueous humor flow through the ciliary muscle and suprachoroidal space. Ocular hypertension occurs when one or both of these pathways of aqueous humor outflow are interrupted.
The site of greatest outflow resistance has been localized to the juxtacanalicular connective tissue and inner wall of Schlemm's canal.[3] When resistance increases, IOP rises as aqueous continues to be produced at a normal rate.
- Structural changes in the trabecular meshwork contribute to increased outflow resistance. When the balance between matrix synthesis and degradation favors progressive matrix accumulation, the juxtacanalicular region becomes thickened with excess deposition of collagen, fibronectin, and glycosaminoglycans, leading to impaired aqueous outflow.[4][3]
- Biomechanical properties of the trabecular meshwork also influence outflow resistance. Trabecular meshwork endothelial cells can become stiffened as they develop increased actin stress fibers, adopting a more contractile form.[3] When trabecular meshwork cells contract, channel narrowing decreases the capacity to accommodate aqueous outflow.
In summary, the cause of OHTN involves increased trabecular meshwork resistance to aqueous outflow, without alterations to aqueous production or anterior chamber angle anatomy. Age-related structural and cellular changes within the trabecular meshwork—such as accumulation of extracellular matrix and reduced endothelial cell function— lead to chronically elevated IOP in eyes with open angles via impaire outflow through Schlemm canal.
Diagnosis
History
Patients with ocular hypertension are asymptomatic, but they can be identified during examinations by elevated IOP on screening tonometry. A comprehensive history should focus on identifying risk factors for progression to glaucoma. Important historical elements include:
- Family History: A detailed family history should document any first-degree relatives with glaucoma or ocular hypertension.
- Previous IOP Measurements: Review any available readings from previous appointments. This can establish whether the elevated pressure is new or longstanding.
- Current Medications: A thorough medication history including any prior use of IOP-lowering medications and corticosteroid use. Steroid-induced ocular hypertension can occur in susceptible individuals.[5]
- Prior Ocular Trauma or Surgery: Previous ocular trauma can cause angle recession or trabecular meshwork damage, while surgical procedures may alter aqueous dynamics or leave residual debris that affects outflow.[6]
- Prior Gonioscopy Results: Previous gonioscopy findings should be documented. Angle anatomy influences both IOP elevation risk and management decisions.[5]
- Systemic Medical History: Conditions such as diabetes mellitus, systemic hypertension, and cardiovascular disease should be documented and may influence glaucoma risk and treatment decisions.
- Race and Ethnicity: African Americans have an increased risk of developing glaucoma from ocular hypertension.[1][7]
The presence of the risk factors listed above warrants closer monitoring or earlier treatment initiation, as outlined in the Ocular Hypertension Treatment Study and European Glaucoma Prevention Study.[1][7]
Physical Examination
Intial workup includes:
- repeated IOP checks at different times of day to verify elevated IOP is replicable
- Central corneal thickness (CCT)
- Gonioscopy (patient should have normal angle anatomy)
- Dilated exam to examine optic nerve (examine vertical cup-to-disc ratio)
- Baseline disc photos
- Baseline OCT RNFL ± ganglion cell analysis
- Baseline visual fields (preferably 2 reliable tests)
Ocular hypertension is characterized by elevated intraocular pressure (IOP ≥24 mmHg) with normal optic nerves appearance (normal rim thickness, no focal notcing or disc hemorrhage), normal visual fields (no nasal steps, arcuate scatomas, or paracentral loss), and open angles on gonioscopy (absence of angle closure, synechiae, angle ressecion, or cyclodyalysis). The diagnosis of ocular hypertension should be reconsidered if structural or functional changes develop during follow-up. This could indicate conversion to glaucoma.
Differential Diagnosis
Erroneous IOP measument (incorrectly calibrated tonometer, poor tonometry technique), physiologic IOP elevation (diurnal variation, stress, breath holding, valsalva), early primary open angle glaucoma, steroid induced ocular hypertension, pseudoexfoliation syndrome/glaucoma, pigment dispersion syndrome/glaucoma, uveitic glaucoma, traumatic glaucoma, early neovascular glaucoma, phacomorphic/phacolytic glaucoma
Management
There are several risk calculation tools available that estimate the 5 year risk an individual with ocular hypertension will develop POAG based on reults from the Ocular Hypertension Treatment STudy (OHTS) and the European Glaucoma Prevention Study (EGPS): https://ohts.wustl.edu/risk/. These method may be useful clinical tools to aid in determining follow up tesitng and exam frequency in addition to weighting the benefit of starting treatment.[7][8]
General Treatment
General treatment options include observation, starting IOP lowering medication , and selective laser trabeculoplasty (SLT).
Medical Therapy
Topical IOP lowering medication are the mainstay of ocular hypertension management. Prostaglandin anaglogues (latanoprost, bimatoprost, travaporst, tafluprost) are the most common first line therapy option. This is due to the ease of use (once nightly), affodability, superior efficacy (~30% IOP reduction), and favorable side effect profile (coomon side effects: conjunctival hyperemia, periocular skin darkening, eyelash growth). If prostagladin analogues are contraindicated ( history of herpetic keratitis, cosmetic concerns, preganancy), the other ocular hypotenive medication may be utlilized. There include alpha agonists (brimondine, apraclonadine), beta-blockers (timolol, betaxolol, carteolol, levobunolol), carbonic anhydrase inhibitors (dorzolamide, brinzolamide), rho kinase inhibitors (netardusil).
Medical Follow-up
Follow up varies depending on risk assesment and physician preferance:
- For low risk individuals, IOP check may be repated very 6 to 12 month and a comprehensive dialted exam may be repated annually. Repeated OCT RNFL/ganglion cell analysis and visual feild testing every 1 to 2 yeats may be sufficient. [9]
- For higher risk individuals, closer follow up very 4 to 6 months with repeat IOP checks and optic nerve exams may be neccesary. OCT RNFL/ganglion cell analysis and visual field testing is recommneded the be repeated every 6 to 12 months.[9]
- If IOP lowering medication is initiated, follow up visit for IOP check in 4 to 6 weeks is recommned.
Procedures and Surgery
Selective laser trabeculoplasty (SLT) is an established, safe, and effective option for lowering intraocular pressure in patients with ocular hypertension. Evidence from the Laser in Glaucoma and Ocular Hypertension (LiGHT) Trial demonstrated that, over six years of follow-up, initial treatment with SLT resulted in sustained intraocular pressure control, reduced reliance on topical medications, and lower overall treatment costs, without an increased risk of sight-threatening adverse events. These findings support the use of SLT as an appropriate first-line treatment option for selected patients with ocular hypertension. [10]
There are no recommneded surgical options specifically for the treatment of ocular hypertension. In patients with visually significant cataracts and ocular hypertension, catarct surgery can be considered as cataract removal has shown to result in sustained IOP reduction. [11]
Prognosis
The prognosis for individuals with ocular hypetension is favorable as demostated by the Ocular Hyptertention Treatment Study (OHTS) and the European Glaucoma Prevention Study (EGPS).[1][2] Ocular hypertension is a slowly progrssive or nonprogressive conditions. Most patients never develop glaucoma, and patients who do generally converted late and with mild disease. Early treatment primarily benefits patients with identifiable high-risk features.
In the OHTS, approximately 9.5% of untreated patients converted to glaucoma, while treatment with topical ocular hypotensive medications reduced the conversion rate by about half, to 4.4% over a 5 year follow up period.[1] Long-term follow-up extending to approximately 20 years showed that about 45% of participants eventually developed glaucoma[1]. When conversion occurred, it was typically delayed and characterized by early, mild disease rather than advanced visual field loss or blindness. Early treatment delayed the onset of glaucoma but did not eliminate lifetime risk, underscoring that treatment modifies timing rather than susceptibility.[1][2] Prognosis was strongly risk-dependent: individuals with lower baseline risk—such as those with thicker central corneas, lower intraocular pressure, smaller cup-to-disc ratios, and younger age—had an excellent prognosis with observation alone, whereas higher-risk patients derived meaningful benefit from early treatment.[1][2] A notable limitation of the OHTS and EGPS is that optical coherance tomography of the retinal nerve fiber layer (OCT RNFL) was not utilized, potentially leading to underestimation of the true conversion rate of OHTN to POAG.
Additional Resources
Ocular Hypertension Risk Calculator: https://ohts.wustl.edu/risk/
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 Kass MA, Heuer DK, Higginbotham EJ, et al. 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
- ↑ 2.0 2.1 2.2 2.3 Miglior S, Zeyen T, Pfeiffer N, Cunha-Vaz J, Torri V; European Glaucoma Prevention Study Group. Results of the European Glaucoma Prevention Study. Ophthalmology. 2005;112(3):366-375. doi:10.1016/j.ophtha.2004.10.020
- ↑ 3.0 3.1 3.2 Tamm ER, Braunger BM, Fuchshofer R. Intraocular pressure and the mechanisms involved in resistance of the aqueous humor flow in the trabecular meshwork outflow pathways. Prog Mol Biol Transl Sci. 2015;134:301-314. doi:10.1016/bs.pmbts.2015.06.007
- ↑ Goel M, Picciani RG, Lee RK, Bhattacharya SK. Aqueous humor dynamics: a review. Open Ophthalmol J. 2010;4:52-59. doi:10.2174/1874364101004010052
- ↑ 5.0 5.1 Fini ME, Schwartz SG, Gao X, et al. Steroid-induced ocular hypertension/glaucoma: Focus on pharmacogenomics and implications for precision medicine. Prog Retin Eye Res. 2017;56:58-83. doi:10.1016/j.preteyeres.2016.09.003
- ↑ Paulavičiūtė-Baikštienė D, Baršauskaitė R, Janulevičienė I. New insights into pathophysiological mechanisms regulating conventional aqueous humor outflow. Medicina (Kaunas). 2013;49(4):26. doi:10.3390/medicina49040026
- ↑ 7.0 7.1 7.2 Gordon MO, Torri V, Miglior S, et al; Ocular Hypertension Treatment Study Group; European Glaucoma Prevention Study Group. A validated prediction model for the development of primary open-angle glaucoma in individuals with ocular hypertension. Ophthalmology. 2007;114(1):10-19.e2. doi:10.1016/j.ophtha.2006.08.031
- ↑ Clinical decision-making algorithms for glaucoma. Glaucoma Education Center; ONE Network; American Academy of Ophthalmology.
- ↑ 9.0 9.1 American Academy of Ophthalmology. Primary Open-Angle Glaucoma Suspect Preferred Practice Pattern®. San Francisco, CA: American Academy of Ophthalmology; 2020. Accessed [date]. https://www.aao.org/preferred-practice-pattern/primary-open-angle-glaucoma-suspect-ppp
- ↑ Gazzard G, Konstantakopoulou E, Garway-Heath D, et al; LiGHT Trial Study Group. Laser in Glaucoma and Ocular Hypertension (LiGHT) Trial: six-year results of primary selective laser trabeculoplasty versus eye drops for the treatment of glaucoma and ocular hypertension. Ophthalmology. 2023;130(2):139-151. doi:10.1016/j.ophtha.2022.08.010
- ↑ Mansberger SL, Gordon MO, Jampel H, et al. Reduction in intraocular pressure after cataract extraction: the Ocular Hypertension Treatment Study. Ophthalmology. 2012;119(9):1826-1831. doi:10.1016/j.ophtha.2012.02.050
