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Moran CORE | Ocular Hypertension

Home / Glaucoma

Title: Ocular Hypertension
Authors: J. Michael Swink, BS; William Clark, BA; Brian Stagg, MD MS
Date: 07/07/2020
Keywords/Main Subjects: Glaucoma, Ocular Hypertension, Ocular Hypertension Treatment Study

Introduction and Definition:

Ocular hypertension (OHT) is the generic term used when a patient has an intraocular pressure (IOP) greater than 21 mmHg with no sign of visual field impairment nor optic disc damage.1 It is one of the leading modifiable risk factors for development of glaucoma.2

Key Features:

For patients with OHT, their eye appears normal with an open anterior chamber angle on gonioscopic examination.  On fundus exam and imaging, there is no manifestation of damage to the ocular nerve. The anterior chamber is open on gonioscopic examination. Visual field findings are also normal on examination of a patient with OHT.1

Landmark Study: The Ocular Hypertension Treatment Study (OHTS)

The OHTS study was conducted from 1997 to 2002 with 1636 participants between the ages of 40 and 80. This sample population had OHT with no evidence of glaucomatous damage. Patients were selected based on their IOP (between 24 and 32 mmHg in one eye and 31 and 32 mmHg in the other eye). Patients that had evidence of ocular damage, poor visual acuity (less than 20/40), a history of intraocular surgery outside of cataract surgery and posterior chamber lens implantation, and optic disc-damaging conditions such as diabetic retinopathy were excluded from the study.

Study participants were randomized to an observational group or the treatment group. Treatment regimens consisted of all hypotensive drops in the US, with new drops added as they became commercially available.  The target goal of the treatment group was to reach an IOP of 24 mmHg or less or to reduce IOP by 20% from their average qualifying and baseline IOP measurements. Drops were added, dropped and changed at physician discretion until target goals were met. Drop regimens consisted of beta-adrenergic antagonists, prostaglandin analogues, topical carbonic anhydrase inhibitors, alpha-2 adrenergic agonists, parasympathomimetic agents, and epinephrine/dipivefrin.

Patients were observed at six-month intervals for 72 to 78 months where IOP was measured and they were checked for visual field loss and intraocular damage. This study found that the use of topical IOP-lowering medications in ocular hypertensive individuals reduced the risk of glaucoma development from 9.5% in the control group to 4.4% in the intervention group.3

Risk Factors for developing OHT:

As people age, IOP naturally increases, putting elderly patients more at risk of developing ocular hypertension.4 A positive family history of glaucoma has also been shown to be a risk factor for developing OHT in Latino populations.5

Complications from OHT:

One of the main risks of uncontrolled OHT is conversion to glaucoma.6  Central corneal thickness (CCT) is a significant risk factor for conversion. Patients thin/low CCT measurements (less than 555 micrometers) are at higher risk of OHT transformation to glaucoma than those with high CCT values (greater than 488 micrometers).7 A greater cup to disc ratio on fundus examination is another statistically significant risk for glaucomatous development.8,9

Other risk factors for glaucoma conversion include age, race (African ethnic background is a predisposing factor), gender (males are at higher risk), and pre-existing heart disease. Studies have found factors such as myopia, diabetes, and a family history of glaucoma to be statistically insignificant.6

OHT has also been described as a risk factor for the development of branched retinal venous occlusion (BRVO) and central retinal venous occlusion (CRVO).10–12

Genetic Factors:

112 genetic loci have been associated with modifying IOP. Many of the genetic risk factors for OHT are similar to those found in glaucoma. Genes such as CYP1B1, MYOC, FOXC1, and PITX2 are all associated with the development of high-pressure glaucoma. Recently, a single nucleotide polymorphism in the TMC01 gene has been associated with increased risk for conversion to glaucoma in non-Hispanic white populations.13,14

Symptoms and Pathophysiology:

Patients with OHT are generally asymptomatic until the condition converts into glaucomatous disorders. It is usually discovered incidentally on ophthalmic examination.6 OHT is the result of impaired aqueous fluid drainage out of the front the eye via the trabecular meshwork. A higher intraocular pressure is required to drain the aqueous humor, leading to a chronically elevated IOP.15

Differential Diagnosis:

Undiagnosed glaucoma in one of its many forms should be considered when evaluating a patient for ocular hypertension. The most notable of these is primary open-angle glaucoma (POAG), but it may also be a manifestation of secondary open angle glaucoma, angle recession glaucoma, or chronic angle closure glaucoma (CACG).1,16

Topical or systemic corticosteroid use is an iatrogenic cause of secondary OHT.17 There is also evidence that use of anti-vascular endothelial growth factor (anti-VEGF) drugs used to treat neovascular macular degeneration can also increase intraocular pressure.18 Infectious keratitis has also been linked to elevated IOP measurements and poor outcomes.19

Other causes of damage to the optic nerve such as drusen, ischemia, venous occlusion, and macular degeneration should also be ruled out when evaluating patients with OHT.1

Clinical Evaluation and Diagnosis:

Clinical evaluation of ocular hypertension is similar to a glaucoma evaluation. A comprehensive history is an important component of the examination. Clinicians should pay particular attention to the patient’s age, race, medication history (steroid use), past medical history (heart disease), past surgical history and prior ocular history.

Baseline examination should include visual acuity and pupillary assessment, gonioscopy, applanation tonometry, and baseline visual fields. If there is no evidence of angle closure, a dilated fundus examination should be performed.16

Pachymetry can also be a useful tool for patients with possible OHT; thicker corneas lead to an overestimation of IOP. Formal visual field testing (IE automated perimetry) establishes baseline visual fields and can be useful for monitoring disease progression. Optic nerve imaging should also be performed to rule out any nerve damage.

Management, Course, and Outcome:

OHT can be managed either by treating the condition or by regular observation. Treatment of choice is usually beta-agonist or prostaglandin eyedrops administered once daily. Outcomes and effectiveness of ocular hypotensive medication are directly correlated with patient adherence.20 Laser treatment and stent placement are other options available to patients that have been shown to lower IOP.21–23 Treating OHT lowers the glaucoma conversion risk from 9.5% to 4.4% after five years.24

There is much discussion, however, on whether or not every patient with ocular hypertension needs to be treated. Studies have shown that higher-risk patients benefit more from treatment than low-risk individuals. Factors such as age, life expectancy, and patient preference should also be considered in the treatment decision.25 Current guidelines do not set a standard IOP that should be treated. They instead urge clinicians to consider IOP along with other patient risk factors when deciding to treat a patient.1  Risk calculator are available to assess OHT patients. These calculators can help clinicians and patients make a joint decision regarding treatment.26,27

Careful follow-up with OHT patients can help prevent future visual field loss. If medications are started, reexamination should occur every 4-6 weeks until IOP is reduced adequately. Once IOP has been reduced, the patient is generally reexamined every 3-6 months. If there is no disease progression, monitoring frequency should be reduced to every 6-12 months. Annual retinal exams, gonioscopy, and formal visual fields should also be performed on high risk patients with OHT.1

Format: Text

References:

  1. Prum BE, Lim MC, Mansberger SL, et al. Primary Open-Angle Glaucoma Suspect Preferred Practice Pattern® Guidelines. Ophthalmology. 2016;123(1):P112-P151. doi:10.1016/j.ophtha.2015.10.055
  2. Rupp JD, Kass MA. Ocular Hypertension. In: Ophthalmology. 5th ed. ; 2019:1055-1056.e1. Accessed June 18, 2020. http://www.clinicalkey.com/#!/content/book/3-s2.0-B9780323528191001511
  3. 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
  4. Baek SU, Kee C, Suh W. Longitudinal analysis of age-related changes in intraocular pressure in South Korea. Eye. 2015;29(5):625-629. doi:10.1038/eye.2015.11
  5. Doshi V, Ying-Lai M, Azen SP, Varma R, Los Angeles Latino Eye Study Group. Sociodemographic, family history, and lifestyle risk factors for open-angle glaucoma and ocular hypertension. The Los Angeles Latino Eye Study. Ophthalmology. 2008;115(4):639-647.e2. doi:10.1016/j.ophtha.2007.05.032
  6. 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. doi:10.1001/archopht.120.6.714
  7. Brandt JD, Beiser JA, Kass MA, Gordon MO. Central Corneal Thickness in the Ocular Hypertension Treatment Study (OHTS). Ophthalmology. 2020;127(4):S72-S81. doi:10.1016/j.ophtha.2020.01.028
  8. Salmon JF. Glaucoma. In: Kanski’s Clinical Ophthalmology. 9th ed. ; 2020:345-422. Accessed May 29, 2020. http://www.clinicalkey.com/#!/content/book/3-s2.0-B978070207711100011X?scrollTo=%23hl0001327
  9. Medeiros FA, Alencar LM, Zangwill LM, Sample PA, Weinreb RN. The Relationship between Intraocular Pressure and Progressive Retinal Nerve Fiber Layer Loss in Glaucoma. Ophthalmology. 2009;116(6):1125-33.e1-3. doi:10.1016/j.ophtha.2008.12.062
  10. Jaulim A, Ahmed B, Khanam T, Chatziralli IP. BRANCH RETINAL VEIN OCCLUSION: Epidemiology, Pathogenesis, Risk Factors, Clinical Features, Diagnosis, and Complications. An Update of the Literature. Retina. 2013;33(5):901-910. doi:10.1097/IAE.0b013e3182870c15
  11. Hayreh SS, Zimmerman MB, Beri M, Podhajsky P. Intraocular pressure abnormalities associated with central and hemicentral retinal vein occlusion. Ophthalmology. 2004;111(1):133-141. doi:10.1016/j.ophtha.2003.03.002
  12. Barnett EM, Fantin A, Wilson BS, Kass MA, Gordon MO. The Incidence of Retinal Vein Occlusion in the Ocular Hypertension Treatment Study. Ophthalmology. 2010;117(3):484-488. doi:10.1016/j.ophtha.2009.08.022
  13. Scheetz TE, Faga B, Ortega L, et al. Glaucoma Risk Alleles in the Ocular Hypertension Treatment Study (OHTS). Ophthalmology. 2016;123(12):2527-2536. doi:10.1016/j.ophtha.2016.08.036
  14. Ojha P, Wiggs JL, Pasquale LR. The Genetics of Intraocular Pressure. Semin Ophthalmol. 2013;28(5-6):301-305. doi:10.3109/08820538.2013.825291
  15. Villamarin A, Roy S, Hasballa R, Vardoulis O, Reymond P, Stergiopulos N. 3D simulation of the aqueous flow in the human eye. Med Eng Phys. 2012;34(10):1462-1470. doi:10.1016/j.medengphy.2012.02.007
  16. The Wills Eye Manual : Office and Emergency Room Diagnosis and Treatment of Eye Disease. Accessed June 17, 2020. http://web.b.ebscohost.com.ezproxy.lib.utah.edu/ehost/ebookviewer/ebook?sid=acda6ef5-dd70-4171-98d2-f002749be023%40pdc-v-sessmgr04&vid=0&format=EK
  17. 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
  18. Moraru A, Pînzaru G, Moţoc A, Costin D, Brănişteanu D. Incidence of ocular hypertension after intravitreal injection of anti-VEGF agents in the treatment of neovascular AMD. Romanian J Ophthalmol. 2017;61(3):207-211.
  19. Sakiyalak D, Chattagoon Y. Incidence of and risk factors for secondary ocular hypertension in moderate to severe infectious ulcerative keratitis. Clin Ophthalmol Auckl NZ. 2018;12:2121-2128. doi:10.2147/OPTH.S169280
  20. Campbell JH, Schwartz GF, LaBounty B, Kowalski JW, Patel VD. Patient adherence and persistence with topical ocular hypotensive therapy in real-world practice: a comparison of bimatoprost 0.01% and travoprost Z 0.004% ophthalmic solutions. Clin Ophthalmol Auckl NZ. 2014;8:927-935. doi:10.2147/OPTH.S49467
  21. Ma A, Yu SWY, Wong JKW. Micropulse laser for the treatment of glaucoma: A literature review. Surv Ophthalmol. 2019;64(4):486-497. doi:10.1016/j.survophthal.2019.01.001
  22. Lavia C, Dallorto L, Maule M, Ceccarelli M, Fea AM. Minimally-invasive glaucoma surgeries (MIGS) for open angle glaucoma: A systematic review and meta-analysis. PLoS ONE. 2017;12(8). doi:10.1371/journal.pone.0183142
  23. Selective laser trabeculoplasty versus eye drops for first-line treatment of ocular hypertension and glaucoma (LiGHT): a multicentre randomised controlled trial- ClinicalKey. Accessed May 29, 2020. https://www.clinicalkey.com/#!/content/journal/1-s2.0-S014067361832213X
  24. Gordon MO, Kass MA. What we have learned from the Ocular Hypertension Treatment Study. Am J Ophthalmol. 2018;189:xxiv-xxvii. doi:10.1016/j.ajo.2018.02.016
  25. 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. Published online 2008. doi:10.1097/IJG.0b013e3181659e6a
  26. 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
  27. Risk Calculator | Ocular Hypertension Treatment Study (OHTS). Accessed June 17, 2020. https://ohts.wustl.edu/risk/

Faculty Approval by: Brian Stagg, MD, MS

Identifier: Moran_CORE_29606

Copyright statement: Copyright ©2020. For further information regarding the rights to this collection, please visit: http://morancore.utah.edu/terms-of-use/

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