Hypertension

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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Nov 9, 2016 | Posted by in OPHTHALMOLOGY | Comments Off on Hypertension

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