History
In the evaluation of ocular hypertension, details should be obtained with respect to the following:
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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 [24]
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Past medical history - Any surgeries or pertinent vascular illnesses, such as cardiovascular disease, diabetes mellitus, migraine headache, hypertension, and vasospasm [25]
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Current medications - Hypertensive medications (which may indirectly cause fluctuation of IOP) or topical/systemic corticosteroids [26]
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Known risk factors for glaucomatous optic neuropathy (POAG) should also be assessed, such as personal history of elevated IOP, advanced age (>50 y), African American descent, myopia, and positive family history/severity of glaucoma in a first-degree relative [27]
Physical Examination
A comprehensive eye examination, such as that outlined in the American Academy of Ophthalmology (AAO) Preferred Practice Patterns, should be performed. [28] Emphasis should be on ruling out early POAG or secondary causes of glaucoma. [29] See the image below.
Flowchart for evaluation of a patient with suspected glaucoma. Used by permission of the American Academy of Ophthalmology.
Visual acuity should be assessed. In isolated ocular hypertension, vision remains normal.
Pupils should be assessed. Afferent pupillary defect (Marcus-Gunn) status should be determined. Ideally, pupil size should be documented at the time of visual-field testing since miosis may mimic early visual-field loss.
Slit-lamp examination of the anterior segment
With regard to the cornea, signs of microcystic edema can be found with a sudden elevation of IOP. Keratic precipitates, pigment on the endothelium (Krukenberg spindle), and congenital and other anomalies suggest a secondary cause of elevated IOP.
For the anterior chamber, assess for an absence of cell or flare, hyphema, foreign bodies, and angle closure.
For the iris, assess for an absence of transillumination defects, iris atrophy, synechiae, rubeosis, ectropion uveae, iris bombé, difference in iris coloration bilaterally (eg, Fuchs heterochromic iridocyclitis), or pseudoexfoliation (PXF) material.
For the lens, assess for an absence of phacomorphic, PXF, Morgagnian, or phacolytic cataract.
Gonioscopy
Gonioscopy should be performed to rule out angle closure or secondary causes of IOP elevation, such as angle recession, pigmentary glaucoma, or PXF.
Fundus examination
Stereoscopic examination of the optic nerves should be performed, looking for the following possible signs of glaucomatous damage [30] :
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Enlarged cup-to-disc ratio in the horizontal and vertical meridians
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Progressive enlargement of the cup
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Evidence of nerve fiber layer damage with red-free filter
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Notching or thinning of the disc rim, particularly at the superior and inferior poles
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Pallor
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Presence of hemorrhage, most common inferotemporally
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Asymmetry of cup-to-disc ratio between eyes
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Peripapillary atrophy
Note the images below.
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 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.
Other fundus abnormalities that could account for any nonglaucomatous visual-field defects or vision loss (eg, disc drusen, optic pits, macular disease, retinopathy) should be noted.
Tonometry
When checking IOP, record measurements for both eyes, the method used (eg, Goldmann applanation, Tono-Pen, pneumotonometer), and the time the measurement was taken.
Considerations in assessing tonometry measurements are as follows:
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Is the reading reproducible?
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What method was used to obtain the reading?
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What was the time of day?
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Do both eyes have similar measurements?
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Is the tonometry value adjusted for corneal pachymetry?
In patients who are obese or anxious, consider the possibility of a Valsalva movement causing increased IOP when measured with the slit lamp by Goldmann applanation. If so, measurement should be tried via the Tono-Pen or Perkins tonometer or a pneumotonometer with the patient resting back in the examination chair.
Goldmann applanation is considered the criterion standard. [31, 32, 33, 34] However, in cases of increased corneal or scleral rigidity (eg, status post [S/P] keratoplasty, scleral buckle), pneumotonometry or a Tono-Pen measurement can be used and may be more accurate. [35]
IOP varies from hour to hour in any individual. The circadian rhythm of IOP usually causes it to rise in the early hours of the morning; IOP also rises with a supine posture, possibly more so in ocular hypertensive patients.
A difference between eyes of 3 mm Hg or more indicates a greater likelihood of glaucoma. Review previous tonometry readings, if available. Expect an average difference of 10% between individual measurements. 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. [29]
Studies such as the OHTS have suggested that applanation pressures vary significantly according to corneal thickness and that some patients diagnosed with ocular hypertension actually may be normotensive when correction is made for central corneal thicknesses CCTs. [36, 37, 38] IOP measurements should be interpreted in the context of pachymetry measurements.
Pachymetry
Pachymetry is used to measure CCT and is known to influence applanation tonometry values. [31, 39] (See the image below.)
According to the OHTS, pachymetry is now the criterion standard for every baseline examination in patients who are at risk for or are suspected of having glaucoma. [4, 40]
Visual-field/automated perimetry testing
Automated perimetry testing (eg, Humphrey 24-2 visual-field test) should be performed to rule out any glaucomatous visual-field defects. (See the image below.) If there are any visual-field or optic nerve changes consistent with early glaucoma, the patient should no longer be referred to as having ocular hypertension. [41, 42]
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.
Considerations in visual-field testing
Visual-field defects may not be apparent until more than 40% loss of the nerve fiber layer has occurred. New-onset glaucomatous defects in an individual with previously diagnosed ocular hypertension are found most commonly as an early nasal step, a temporal wedge, or a paracentral scotoma (more frequently superiorly). Generalized depression also can be found. See the image below.
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.
Pupillary constriction can reduce retinal sensitivity and mimic field loss.
Software based on the Swedish interactive thresholding algorithm (SITA) may decrease testing time and boost reliability, especially in older patients. Short-wavelength automated perimetry (SWAP) testing, or blue-yellow perimetry, has been proposed as a more sensitive method of detecting visual-field deficits in patients diagnosed with ocular hypertension. Some studies have suggested 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. [43, 44, 45] Because testing time is lengthened, it may be tiring for some patients; newer SITA-SWAP software was developed to speed up the testing time and thus improve reliability. [46] Some studies have not found SITA-SWAP to be better than standard perimetry testing. [47]
The initial visual field may need to be repeated at least twice on successive visits if initial testing shows low reliability indices. Newer glaucoma progression analysis (GPA) software can help to identify reliable perimetric baselines, and probability-based analyses of subsequent fields can assist in determining if there is true progression over time versus artifact. [48] If the patient is unable to perform automated testing, manual Goldmann perimetry testing may be substituted.
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Diagram of intraocular pressure distribution. Used with permission from Survey of Ophthalmology.
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Flowchart for evaluation of a patient with suspected glaucoma. Used by permission of the American Academy of Ophthalmology.
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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
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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.
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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.
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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.
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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.
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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.
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Advanced glaucomatous damage with increased cupping and substantial pallor of the optic nerve head. Courtesy of M. Bruce Shields.
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Correction values according to corneal thickness.
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Ocular hypertension study (OHTS). Percentage of patients who developed glaucoma during this study, stratified by baseline intraocular pressure (IOP) and central corneal thickness (CCT).
