BASICS
DESCRIPTION
Elevated intraocular pressure (IOP >21 mm Hg) with normal anterior chamber angle and anatomy and no evidence of optic nerve or visual field damage
EPIDEMIOLOGY
Incidence
Unknown
Prevalence
4–7% of individuals older than 40 years.
RISK FACTORS
• No specific risk factors identified
• Risk factors for subsequent development of primary open-angle glaucoma include increased age, IOP, cup to disc ratio, and pattern standard deviation (PSD) on visual field testing as well as thinner central corneal thickness (CCT) (1,2)[A].
Genetics
• No specific markers yet identified.
• An association study of Ocular Hypertension Treatment Study (OHTS) participants is underway.
GENERAL PREVENTION
No preventative measures known but routine eye exams result in earlier identification, monitoring, and intervention if glaucomatous damage occurs.
PATHOPHYSIOLOGY
Unknown but may share features with primary open-angle glaucoma
ETIOLOGY
Unknown but may share features with primary open-angle glaucoma
COMMONLY ASSOCIATED CONDITIONS
• Increased CCT
• Primary open-angle glaucoma
DIAGNOSIS
HISTORY
Asymptomatic
PHYSICAL EXAM
• Elevated IOP with gonioscopically normal anterior chamber angle and anatomy
• No corneal edema, anterior chamber reaction, or conjunctival injection
• No detectable optic nerve or visual field damage
DIAGNOSTIC TESTS & INTERPRETATION
Imaging
Initial approach
Optic nerve head analysis (e.g., Heidelberg retina topography [HRT] or optical coherence tomography [OCT]) will be normal in ocular hypertension but abnormal in primary open-angle glaucoma.
Follow-up & special considerations
Serial evaluation of the optic nerve head is necessary to detect subsequent glaucomatous damage and initiate or alter treatment.
Diagnostic Procedures/Other
• Pachymetry—thinner corneas yield falsely low IOP readings, and thicker corneas yield falsely high IOPs.
• Visual field testing—if abnormal and consistent with optic nerve findings, suspect primary open-angle glaucoma.
Pathological Findings
None–-hallmark of ocular hypertension is elevated IOP without detectable damage.
DIFFERENTIAL DIAGNOSIS
• Primary open-angle glaucoma—damage to the nerve and visual field
• Secondary open-angle glaucoma—other associated findings such as inflammation, pigment dispersion, or pseudoexfoliation
• Chronic angle-closure glaucoma—peripheral anterior synechiae and damage to the nerve and visual field
TREATMENT
MEDICATION
First Line
If treatment and not observation is planned, topical prostaglandin analogue or beta-blocker is preferred (3,4)[A].
Second Line
Topical carbonic anhydrase inhibitor or alpha-adrenergic agonist
ADDITIONAL TREATMENT
General Measures
The decision to treat or monitor closely in the absence of glaucomatous damage is complicated and requires discussion with the patient and evaluation of risk factors for open-angle glaucoma.
Additional Therapies
Laser trabeculoplasty is often considered a first-line treatment option or as an adjunct to topical medications.
SURGERY/OTHER PROCEDURES
• Laser trabeculoplasty
• Trabeculectomy if progression and laser or medical therapy insufficient
• Aqueous tube shunt if progression and laser or medical therapy insufficient
ONGOING CARE
FOLLOW-UP RECOMMENDATIONS
Initially patients, whether treated or not, should be monitored every 3–4 months according to the standard follow-up for primary open-angle glaucoma.
Patient Monitoring
If no damage occurs in the first few years, the frequency of monitoring can be reduced to every 6–12 months.
PATIENT EDUCATION
Patients should understand the importance of monitoring and the increased risk of the development of open-angle glaucoma.
PROGNOSIS
• In 5 years, approximately 10% of untreated patients with ocular hypertension greater than 24 mm Hg will develop glaucoma.
• 4.4% cumulative risk of glaucoma development with treatment group; 9.5% without treatment (3)[A]
COMPLICATIONS
Development of glaucomatous optic nerve and visual field damage
REFERENCES
1. Gordon MO, Beiser JA, Brandt JD, et al. The Ocular Hypertension Treatment Study: Baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol 2002;120(6):714–720; discussion 829–830.
2. Brandt JD SL, Beiser JA, Kass MA, et al. Ocular Hypertension Treatment Study Group. Central corneal thickness in the Ocular Hypertension Treatment Study (OHTS). Ophthalmol 2001;108(10):1779–1788.
3. Mansberger SL, Hughes BA, Gordon MO, et al. Ocular Hypertension Treatment Study Group. Comparison of initial intraocular pressure response with topical beta-adrenergic antagonists and prostaglandin analogues in African American and white individuals in the Ocular Hypertension Treatment Study. Arch Ophthalmol 2007;125(4):454–459
4. 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; discussion 829–830.
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