Ocular Hypertension 

  • Author: Jerald A Bell, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Jan 5, 2011
 

Background

The term ocular hypertension (OHT) often has been used as a generic term, referring to any situation in which intraocular pressure (IOP) is greater than 21 mm Hg. Such usage could refer to a variety of conditions in which it occurs (eg, traumatic hyphema, orbital edema, postoperative viscoelastic retention, intraocular inflammation, corticosteroid use, pupillary block, idiopathic causes). The term makes no mention of whether or not glaucomatous nerve damage is present. It also depicts no particular time frame during which the elevated pressure has been measured. Consequently, clarification of the term is the first topic of mention.

The definition of this condition has evolved throughout the latter part of the 20th century.[1] It was used as early as 1962 by Drance, but it was not defined in English language publications until 1966 by Perkins and others, with definitions similar to the following:

Ocular hypertension is a condition in which the below criteria are present:

  • An intraocular pressure greater than 21 mm Hg in one or both eyes as measured by applanation tonometry on 2 or more occasions
  • No glaucomatous defects on visual field testing
  • Normal appearance of the optic disc and nerve fiber layer
  • Open angles on gonioscopy, with no history of angle closure
  • Absence of any ocular disease contributing to the elevation of pressure

Beginning in the 1970s, controversy began to erupt on the usefulness of the term. Despite the clear-cut early definitions, ocular hypertension had come to mean different things to different people.[1] Ophthalmologists became concerned with the ambiguity of the term. People, such as Hitchings, began to stress the point of not reading too much into the term, as its definition "does not imply an ocular hypertensive will not develop glaucoma, nor does this label imply that an early stage of glaucoma exists (see the image below).[2] Such a patient with this label may remain without other signs of glaucoma, or may become normotensive, or may develop glaucomatous cupping with or without field loss, and become a case of frank glaucoma."

Diagram showing the relative proportion of people Diagram showing the relative proportion of people in the general population who have elevated pressure (horizontally-shaded lines) and/or damage from glaucoma (vertically-shaded lines). Notice that most have elevated pressure but no sign of damage (ie, ocular hypertensives), but there are those with normal pressures who still have damage from glaucoma (ie, normal tension glaucoma). (Diagram used by permission of M. Bruce Shields.) OHT = horizontal lines only NTG = vertical lines only POAG and other glaucomas with both elevated intraocular pressure and damage = overlapping horizontal and vertical lines

Consequently, since the late 1970s, several (including George Spaeth) have advocated total disuse of the term, secondary to this inherent ambiguity or what has been called an elegant hedge. They feel such a term implies that the physician has future knowledge of the patient's course, when, in fact, the opposite is true. Hence, they prefer the term glaucoma suspect, which is believed to more adequately convey the uncertainty regarding the diagnosis and prognosis.[3] On the other hand, many feel any use of a phrase with the word glaucoma in it implies a malignant meaning, or a certainty that the patient is at a very high risk for developing glaucoma. A classic discussion of what should be appropriate terminology (including even the choice early open-angle glaucoma without damage) can be seen in the multiple editorials by Chandler and Grant, Kolker and Becker, Shaffer, and Phelps in Archives of Ophthalmology dating back to 1977.

In this article, discussion is limited to ocular hypertension as referring to a prolonged state of the eye(s) meeting the above 5 criteria, without other signs of primary open-angle glaucoma (POAG), and from no known specific causation.[4, 5] Ocular hypertension should not be considered as a disease entity by itself, but rather a term describing a subset of individuals who should be observed more closely than the general population for the onset of glaucomatous damage.[6, 7]

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Pathophysiology

Elevated IOP is a great concern in the ocular hypertensive population because it is one of the main risk factors for glaucoma.[8] Elevated IOP is the most studied because it is the main clinically treatable risk factor for glaucoma. Multiple theories discuss how IOP can be one of the factors that initiates glaucomatous damage in a patient. Two of the major theories include the following: (1) onset of vascular dysfunction causing ischemia to the optic nerve, and (2) mechanical dysfunction via cribriform plate compression of the axons.

In addition to vascular compromise and mechanically impaired axoplasmic flow, contemporary hypotheses of possible pathogenic mechanisms that underlie glaucomatous optic neuropathy include excitotoxic damage from excessive retinal glutamate, deprivation of neuronal growth factors, peroxynitrite toxicity from increased nitric oxide synthase activity, immune-mediated nerve damage, and oxidative stress.[9, 10] The exact role that IOP plays in combination with these other factors and their significance as to the initiation and progression of subsequent glaucomatous neuronal damage and cell death over time is still under debate; the precise mechanism is still a hot topic of discussion.[11]

Nevertheless, IOP is the only factor that has been able to be successfully manipulated clinically, so categorizing and managing patients based on their IOP has forced the issue of ocular hypertension and when it should be treated to prevent optic nerve damage.[12]

Several studies over the years have shown that, as IOP rises above 21 mm Hg, the percentage of patients developing visual field loss increases rapidly, most notably at pressures higher than 26-30 mm Hg. A patient with an IOP of 28 mm Hg is about 15 times more likely to develop field loss than an ocular hypertensive with a pressure of 22 mm Hg.[13, 14] Thus, a population described as ocular hypertensive should not be thought of as a homogeneous population.

Before classifying a patient strictly as ocular hypertensive, the following factors should be considered when categorizing where a patient's measurements fall:

  • The variability of tonometry measurements per examiner (usually found to be about 10%, or 1-2 mm Hg)
  • The effect corneal thickness has on accuracy of IOP measurements (see Other Tests)[15, 16]
  • The diurnal variation of IOP (often highest in the early morning hours, but maximum IOP can be at any time of day in some patients)
  • In addition, remember that normal eyes have a diurnal variation of approximately 3-4 mm Hg, while glaucomatous eyes have an even higher variation (>10 mm Hg). Note that multiple readings should be taken over time and should be considered with correlative evidence of visual field and optic nerve examination before any diagnosis or therapy is rendered.

Other points of importance when considering a diagnosis of ocular hypertension include the following:

  • Disc cupping and nerve fiber layer losses of up to 40% have been shown to occur before actual visual field loss has been detected. Therefore, visual field examination cannot be the sole tool used to determine when a patient is no longer ocular hypertensive but, instead, has frank glaucoma, and it should not be used in isolation as the benchmark for treatment.
  • Some evidence suggests ocular hypertensives have a higher variability of IOP with postural changes than in patients with ocular hypertension.
  • Basic and clinical science research continues to look into factors that contribute to the development and prognosis of the ocular hypertensive patient.
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Epidemiology

Frequency

United States

Multiple population studies (including the Framingham, Beaver Dam, Baltimore, Rotterdam, Barbados, and Egna-Neumarkt studies) have been performed to estimate the prevalence of eye disease, including POAG and ocular hypertension.[17]

Estimates of the prevalence of glaucoma in studies involving only the United States suggest the following: glaucoma is a leading cause of irreversible blindness, second only to macular degeneration; only one half of the people who have glaucoma may be aware that they have the disease; and more than 2.25 million Americans aged 40 years and older have POAG. These studies estimate that 3-6 million people in the United States alone, including 4-10% of the population older than 40 years, will have IOPs of 21 mm Hg or higher, without detectable signs of glaucomatous damage using current clinical testing. See the image below.

Diagram of intraocular pressure distribution, withDiagram of intraocular pressure distribution, with a visible skew to the right (somewhat exaggerated compared to the actual distribution). Note that, while uncommon, there can be field loss among individuals with pressures in the upper teens. Also, note how the average pressure among those with glaucoma is in the low 20s, even though most individuals with pressures in the low 20s do not have glaucoma. Used by permission from Survey of Ophthalmology.

Prospective studies over the last 20 years have helped to characterize the ocular hypertensive population.[18] Roughly 0.5-1% per year of those patients with elevated IOP will develop glaucoma over a period of 5-10 years. However, the risk may be even less than 1% per year, now that ophthalmoscopic and perimetric techniques for detecting glaucomatous damage have improved significantly. Ocular hypertension has a 10-15 times greater prevalence than POAG (as defined by visual field loss). Out of every 100 patients older than 40 years, about 10 will have pressures higher than 21 mm Hg, and 1 of those patients will have glaucoma. See Medical therapy versus observation in Medical Care and the images below.[19, 20]

Correction values according to corneal thickness. Correction values according to corneal thickness. Ocular hypertension study (OHTS). Percentage of paOcular hypertension study (OHTS). Percentage of patients who developed glaucoma during this study, stratified by baseline intraocular pressure (IOP) and central corneal thickness (CCT).

International

Glaucoma is the second leading cause of blindness in the world (surpassed only by cataracts, a reversible condition). More than 3 million people are bilaterally blind from POAG worldwide, and more than 2 million people will develop POAG each year.

Mortality/Morbidity

  • Over a 5-year period, several studies have shown the incidence of glaucomatous damage in ocular hypertensives to be about 2.6-3% for IOPs 21-25 mm Hg, 12-26% for IOPs 26-30 mm Hg, and approximately 42% for those higher than 30 mm Hg. The OHTS has further clarified this data. Patients with ocular hypertension have an overall risk of 10% over 5 years of developing glaucoma. This risk can be cut in half by medical treatment. Pachymetry results further stratify this risk into specific subsets.
  • In year 2000, an estimated 2.47 million people in the United States had frank glaucoma and more than 130,000 were legally blind because of this disease. These statistics alone emphasize the need to identify and monitor closely those at risk of glaucomatous damage, especially ocular hypertensives.
  • One specific morbidity associated with ocular hypertension is that of retinal vascular occlusions, which may occur in approximately 3% of ocular hypertensives. It has been suggested that ocular hypertensives older than 65 years be treated to keep their pressures below 25 mm Hg.

Race

  • Black individuals are considered to have a 3-4 times higher prevalence of POAG, and they are believed to be more susceptible to optic nerve damage. There is also a higher prevalence of larger cup-to-disc ratios in the normal black population as compared with white control subjects.
  • The data are more conflicting when it comes to ocular hypertension specifically. Over 4 years, the Barbados Eye Study showed a 5 times higher incidence of developing glaucoma in a group of ocular hypertensives as compared with a predominantly white population.[17]
  • Some population studies have found mean IOP in blacks to be higher than in Caucasian control subjects. Others, such as the Baltimore Eye Study, found no difference. Consequently, further study needs to be completed to clarify this issue.

Sex

Differing reports exist on sexual predilection. Although some age-controlled studies have reported significantly higher mean IOP values in women than in men, others have failed to find such a difference. Some also suggest that although women could be at higher risk for ocular hypertension (especially after menopause), men with ocular hypertension may be at a higher risk for glaucomatous damage.

Age

  • Mean IOP slowly rises with increasing age. Age older than 40 years is considered a risk factor for the development of ocular hypertension and POAG.
  • Elevated pressure in a young person is a cause for concern because an individual would have longer exposure time to high pressures over a lifetime, with more likelihood of developing optic nerve damage.
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Contributor Information and Disclosures
Author

Jerald A Bell, MD  Staff Physician, Department of Ophthalmology, Billings Clinic; Glaucoma Director

Jerald A Bell, MD is a member of the following medical societies: American Academy of Ophthalmology

Disclosure: Nothing to disclose.

Coauthor(s)

Judie F Charlton, MD  Director - Division of Glaucoma, Professor, Department of Ophthalmology, West Virginia University

Judie F Charlton, MD is a member of the following medical societies: American Academy of Ophthalmology

Disclosure: Nothing to disclose.

Specialty Editor Board

Bradford Shingleton, MD  Assistant Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary

Bradford Shingleton, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Ophthalmology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Martin B Wax, MD  Clinical Professor, Department of Ophthalmology, University of Texas Southwestern Medical School; Vice President, Ophthalmology Research and Development, Head, Ophthalmology Discovery Research, Alcon Labs, Inc

Martin B Wax, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Society for Neuroscience

Disclosure: Nothing to disclose.

Lance L Brown, OD, MD  Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD  Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

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Diagram of intraocular pressure distribution, with a visible skew to the right (somewhat exaggerated compared to the actual distribution). Note that, while uncommon, there can be field loss among individuals with pressures in the upper teens. Also, note how the average pressure among those with glaucoma is in the low 20s, even though most individuals with pressures in the low 20s do not have glaucoma. Used by permission from Survey of Ophthalmology.
Flowchart for evaluation of a patient with suspected glaucoma. Used by permission of the American Academy of Ophthalmology.
Diagram showing the relative proportion of people in the general population who have elevated pressure (horizontally-shaded lines) and/or damage from glaucoma (vertically-shaded lines). Notice that most have elevated pressure but no sign of damage (ie, ocular hypertensives), but there are those with normal pressures who still have damage from glaucoma (ie, normal tension glaucoma). (Diagram used by permission of M. Bruce Shields.) OHT = horizontal lines only NTG = vertical lines only POAG and other glaucomas with both elevated intraocular pressure and damage = overlapping horizontal and vertical lines
Humphrey visual field, right eye, showing patient with advanced glaucomatous field loss. Notice both the arcuate extension from the blind spot (Bjerrum scotoma), as well as the loss nasally (nasal step), which often occurs early in the disease process. Courtesy of M. Bruce Shields.
Illustration of progressive optic nerve damage. Notice the deepening (saucerization) along the neural rim, along with notching and increased excavation/sloping of the optic nerve and circumlinear vessel inferiorly. Courtesy of M. Bruce Shields.
Example of progressive visual field loss over time (from top to bottom) in a patient with glaucoma. Notice the early appearance of an inferior nasal step and arcuate loss, with progressive enlargement and increasing density of the scotomata over time. Humphrey visual field courtesy of M. Bruce Shields.
Example of optic nerve asymmetry in a patient with glaucomatous damage, left eye, showing optic nerve excavation inferiorly similar to Image 5. Used by permission of M. Bruce Shields.
Glaucomatous optic nerve damage, with sloping and nerve fiber layer rim hemorrhage at the 7-o'clock position. Hemorrhage is indicative of progressive damage, usually due to inadequate pressure control. Further notching and pallor corresponding to the area of hemorrhage usually is seen several weeks after resorption of the blood. Courtesy of M. Bruce Shields.
Advanced glaucomatous damage with increased cupping and substantial pallor of the optic nerve head. Courtesy of M. Bruce Shields.
Correction values according to corneal thickness.
Ocular hypertension study (OHTS). Percentage of patients who developed glaucoma during this study, stratified by baseline intraocular pressure (IOP) and central corneal thickness (CCT).
 
 
 
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