eMedicine Specialties > Ophthalmology > Intraocular Pressure

Ocular Hypertension

Author: Jerald A Bell, MD, Staff Physician, Department of Ophthalmology, Billings Clinic; Glaucoma Director, Leadership Council Member, Physician Advocate for Personal Service Excellence Committee
Coauthor(s): Judie F Charlton, MD, Director - Division of Glaucoma, Professor, Department of Ophthalmology, West Virginia University
Contributor Information and Disclosures

Updated: Nov 10, 2008

Introduction

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. 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. 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. 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."

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. 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. 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.

See related CME at Treated Open-Angle Glaucoma and Ocular Hypertension Associated With Risk of Cardiovascular-Related Death.

Pathophysiology

Elevated IOP is a great concern in the ocular hypertensive population because it is one of the main risk factors for glaucoma. 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. 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.

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.

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. 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) 
  • 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.

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.

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.

Prospective studies over the last 20 years have helped to characterize the ocular hypertensive population. 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 Media files 10-11.

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.
  • 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.

Clinical

History

The initial patient interview is extremely important in the evaluation of ocular hypertension to detect frank glaucoma or other ocular diseases secondarily causing elevated IOP. Detail should be given to the following:
  • Past ocular history - History of eye pain or redness; multicolored halos; headache; previous ocular disease, including cataracts, uveitis, diabetic retinopathy, and vascular occlusions; previous ocular surgery (including photocoagulation or refractive procedures); or ocular/head trauma
  • Past medical history - Any surgeries or pertinent vasculopathic systemic illnesses
  • Current medications, including any hypertensive medications (which may indirectly cause fluctuation of IOP) or topical/systemic corticosteroids
  • Risk factors for glaucomatous optic neuropathy  
    • Strongly implicated risk factors
      • History of elevated IOP, advanced age (particularly persons >50 y), African American descent, positive family history of glaucoma (first-degree relative; especially correlative if present in a sibling [relative risk 3.7-fold higher than if no family history of glaucoma]), and myopia
      • Be specific when asking family history - Which family members? Did actual visual loss from glaucoma occur? Did other causes of visual field loss occur? Are they under control on one or more medications? Did they require surgery for adequate control?
    • Possibly implicated risk factors - Systemic cardiovascular disease, diabetes mellitus, migraine headache, systemic hypertension, and vasospasm
  • Anecdotal risk factors - Obesity, smoking, alcohol, and history of stress or anxiety (no definitive link to ocular hypertension)

Physical

Screening of the general population for ocular hypertension and POAG is similar, being most effective if targeted toward those at high risk, such as African Americans and elderly persons, especially if the screening consists of IOP measurements combined with assessment of optic nerve status.

Screening should be performed at least every 3-5 years in asymptomatic patients aged 40 years or younger and more often if the person is African American or older than 40 years. For those with multiple risk factors, evaluation/monitoring should be performed on a more frequent basis, as appropriate.

A standard comprehensive eye examination, such as that outlined in the American Academy of Ophthalmology (AAO) Preferred Practice Patterns, should be performed on the initial visit. If there are any visual field or optic nerve changes consistent with early glaucoma, then the patient should be diagnosed as having such and should no longer be referred to as ocular hypertensive.

Emphasis during the examination should be on the following points to rule out early POAG or secondary causes of glaucoma:

  • Visual acuity: Compare visual acuity with previous known acuities (if declining, rule out frank POAG or secondary causes of vision loss, whether from cataracts, age-related macular degeneration [ARMD], ocular surface disorders [eg, dry eye], or adverse effects from topical medications [especially if using miotics]).
  • Pupils: The presence/absence of afferent pupillary defect (Marcus-Gunn) should be seen.
  • Slit lamp examination of the anterior segment
    • Cornea: Look for signs of microcystic edema (found only with a sudden elevation of IOP); keratic precipitates; pigment on endothelium (Krukenberg spindle); and congenital anomalies.
    • Anterior chamber: Examine for cell or flare, uveitis, hyphema, and angle closure.
    • Iris: Transillumination defects, iris atrophy, synechiae, rubeosis, ectropion uveae, iris bombé, difference in iris coloration bilaterally (eg, Fuchs heterochromic iridocyclitis), or pseudoexfoliation (PXF) material may be observed.
    • Lens: Examine for cataract progression (ie, phacomorphic glaucoma, PXF, phacolytic glaucoma with a Morgagnian cataract).
    • Optic nerve/nerve fiber layer: Stereoscopically examine for evidence of glaucomatous damage, including cup-to-disc ratio in horizontal and vertical meridians (describe by color and slope, and diagram, if needed); appearance of disc; progressive enlargement of the cup; evidence of nerve fiber layer damage with red-free filter; notching or thinning of disc rim, particularly at the superior and inferior poles (because nerve fibers at the superior and inferior poles of the disc can often be affected first); pallor; presence of hemorrhage (most common inferotemporally); asymmetry between discs; parapapillary atrophy (possible association with development of glaucoma); or congenital nerve abnormalities.
    • Fundus: Other abnormalities that could account for any nonglaucomatous visual field defects or vision loss present (eg, disc drusen, optic pits, retinal disease), vitreous hemorrhage, or proliferative retinopathy.
  • Baseline stereo fundus photographs: Obtain baseline stereo fundus photographs for future reference/comparison; if unavailable, record representative drawings.
  • Tonometry (see also Tonometric methods in Other Tests) 
    • IOP varies from hour to hour in any individual. The circadian rhythm of IOP usually causes it to rise most in the early hours of the morning; IOP also rises with a supine posture, possibly more so in ocular hypertensives.
    • When checking IOP, record all of the following: measurements for both eyes, the method used (Goldmann applanation is the criterion standard), and the time of the measurement.
    • Review previous tonometry readings, if available (eg, Is the reading reproducible? What method was used to obtain the reading? What was the time of day? Where does it fall on the diurnal pressure curve? Do both the eyes have similar measurements?).
    • In patients who are obese, consider the possibility of a Valsalva movement causing an increased IOP when measured with the slit lamp by Goldmann applanation. Measurement should be tried via Tono-Pen, Perkins, or pneumotonometer with the patient resting back in the examination chair.
    • A difference between the 2 eyes of 3 mm Hg or more indicates a greater likelihood of glaucoma. Expect an average of 10% difference between individual measurements. Repeat the measurements on at least 2-3 occasions before deciding on a treatment plan. Take the measurement in the morning and at night to check the diurnal variation, if possible. (A diurnal variation of more than 5-6 mm Hg may be suggestive of increased risk for POAG.) Early POAG is strongly suspected when a steadily increasing IOP is present.
    • Pachymetry affects applanation tonometry values and, therefore, should be checked on the initial examination.
  • Gonioscopy: Gonioscopy should be performed to rule out angle-closure or secondary causes of IOP elevation, such as angle recession, pigmentary glaucoma, and PXF.
  • Pachymetry: Pachymetry is used to measure central corneal thickness (CCT). According to the OHTS, pachymetry is now the criterion standard for every baseline examination in patients who are at risk for or suspected of having glaucoma (see Media file 11).
  • Visual field testing
    • Perform automated threshold testing (eg, Humphrey 24-2) to rule out any glaucomatous visual field defects. If the patient is unable to perform automated testing, Goldmann testing may be substituted.
    • If the patient is unable to perform automated testing, Goldmann testing may be substituted.
  • Remember the following caveats regarding visual field analysis (see Other Tests):
    • New-onset glaucomatous defects in an individual with previously diagnosed ocular hypertension are found most commonly as an early nasal step, temporal wedge, or a paracentral scotoma (more frequent superiorly); generalized depression related to IOP level also can be found.
    • Swedish interactive thresholding algorithm (SITA)-based software algorithms may decrease testing time and boost reliability, especially in older patients.
    • SWAP (short wavelength automated perimetry or blue-yellow perimetry) may provide a more sensitive method of detecting visual field deficits in those diagnosed as ocular hypertensive. If the Humphrey visual field testing results are normal, SWAP should be considered to help detect visual field loss earlier. Studies suggest that SWAP may detect visual loss/progression up to 3-5 years earlier than conventional perimetry, as well as in 12-42% of patients previously diagnosed with only ocular hypertension. Because the testing time may be lengthened, it may be tiring for some patients. However, new SITA-SWAP algorithm software may speed up the testing time and thus improve reliability.
    • Examination results must take into account that visual field defects may not be apparent until more than 40% loss of the nerve fiber layer has occurred. Therefore, base the therapy on the overall clinical picture and not on visual field testing alone (see Treatment). 
    • Document the pupil size at each testing session, as constriction can reduce retinal sensitivity and mimic progressive field loss.
    • The risk factors, specifically for the development of glaucomatous field loss in ocular hypertension, have been studied, and it was found that several presumed risk factors (ie, presence of hypertension, diabetes, refractive error, race, family history of glaucoma, gender, smoking or ethanol use, disc area) were not found to be of significance for prediction of eventual field loss.
    • Significant positive predictive factors of field loss included higher IOP, older age, presence of a disc crescent, larger cup-to-disc ratio, smaller rim-disc area ratio, and cup asymmetry. Consequently, the relationship of risk factors for ocular hypertension compared with that of actual field loss development is much more complex than has been previously presumed.
    • The initial visual field baseline may need to be repeated at least twice on successive visits, especially if initial testing shows low reliability indices. Newer glaucoma progression analysis (GPA) software can help identify reliable perimetric baselines, and probability-based analyses of subsequent fields can assist in determining if there is true progression over time versus artifact. In follow-up, if there is a low risk of onset of glaucomatous damage, then repeat testing may be performed once a year. If there is a high risk of impending glaucomatous damage, then testing may be adjusted to as frequent as every 2 months.

Causes

See Pathophysiology.

More on Ocular Hypertension

Overview: Ocular Hypertension
Differential Diagnoses & Workup: Ocular Hypertension
Treatment & Medication: Ocular Hypertension
Follow-up: Ocular Hypertension
Multimedia: Ocular Hypertension
References
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Further Reading

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Keywords

ocular hypertension, OHT, intraocular pressure, IOP, glaucoma, primary open angle glaucoma, primary open-angle glaucoma, POAG, Ocular Hypertension Treatment Study, OHTS, high pressure inside the eye, glaucoma suspect, increased IOP, elevated IOP, high IOP, increased intraocular pressure, elevated intraocular pressure, high intraocular pressure, high eye pressure, elevated eye pressure, increased eye pressure, optic nerve, optic nerve damage, visual field defect, vision loss, blindness

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Contributor Information and Disclosures

Author

Jerald A Bell, MD, Staff Physician, Department of Ophthalmology, Billings Clinic; Glaucoma Director, Leadership Council Member, Physician Advocate for Personal Service Excellence Committee
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.

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

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: Alcon Labs Salary Employment

CME Editor

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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