Approach Considerations

A clinical management strategy that targets a 20% reduction in IOP in people with ocular hypertension has been shown to delay or prevent the onset of glaucoma.^[54]

Considering the high average monthly cost of glaucoma medication, along with the possible risks of adverse effects or toxic reactions from drugs, inconvenience of use, and sometimes uncertainty of the overall efficacy of prophylactic therapy, there is strong reason not to treat indiscriminately.^{[55, 56, 57]}The OHTS suggests that treatment of patients with IOP higher than 24 mm Hg among those who have a greater than 2% annual risk of developing glaucoma (see the Prognosis section) is cost-effective.^[58]

Individualization of therapy is the key; an ideal pressure in one patient may cause glaucomatous damage in another person. Periodically reevaluating the target IOP and performing a review of IOP trends and optic nerve anatomy and function via visual-field testing is necessary to determine whether the patient is consistently maintaining his or her ideal pressure.

Medical care

When risk of progression to POAG is present, treatment with IOP-lowering medications is indicated. See Medication.

Surgical care

Generally, if control cannot be achieved with medications, reconsider the diagnosis of ocular hypertension as that of early POAG. Laser and surgical therapy are not viewed as mainstay treatments for ocular hypertension.

Consultations

Referral to a subspecialist fellowship trained in glaucoma and/or neuro-ophthalmology should be considered if there is continued inadequate pressure control, loss of visual acuity, visual-field constriction, optic nerve pallor or cupping, associated systemic conditions, or atypical findings.

Follow Up

Depending on the assessed annual risk of developing glaucoma and level of IOP control, patients may need to be seen at intervals ranging from yearly to every 2 months, or even more frequently if there is a marked lack of IOP control.^[28]

Long-Term Monitoring

Patients should be observed regularly over their lifetime because some are at increased risk for the development of glaucomatous damage. If treated with medications, the potential for adverse effects or toxic reactions from topical medications exists (see Medication).

Medication

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Media Gallery

Diagram of intraocular pressure distribution. Used with 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).