Ocular Hypertension Treatment & Management

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

Medical Care

Some controversy still exists about when to treat ocular hypertension.[56] Some of the questions regarding medical management versus observation have been answered by such studies as the OHTS.

Some physicians incorrectly treat all elevated IOPs higher than 21 mm Hg with topical medication. Other physicians do not treat unless there is evidence of optic nerve damage.[57] Although, as mentioned before, nerve fiber layer loss of up to 40% may occur before visual field defects occur, so do not treat based on visual field testing alone. Most physicians select and treat those patients believed to be at greatest risk for developing glaucoma (most common approach). See History and Physical (visual field testing) for a list of risk factors for glaucomatous field loss.[8, 58]

In any case, the goal of treatment is reduction of the pressure before it causes glaucomatous loss of vision. Some advocate a policy of close observation without treatment simply because most patients are at low risk of visual loss from ocular hypertension.[57] One collaborative glaucoma study showed that only 1.7% of eyes developed visual field loss over a 1- to 13-year period. 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, incidence of noncompliance, and uncertainty of the overall efficacy of prophylactic therapy, there is a strong reason not to treat indiscriminately.[59]

  • Several questions should be asked when considering treatment: Is the elevated pressure significant? Will this patient develop visual loss if left untreated?[60] Is the treatment worth the risk of adverse effects of the medications?
    • One should consider treatment more strongly if the patient reliability or the consequences of missing field loss is an issue (eg, poor reliability on visual field examination, one-eyed patient, poor availability for follow-up care, younger patient, patient whose optic nerve is difficult to visualize, history of vascular occlusion).
    • Treatment is highly recommended if signs of damage consistent with glaucomatous optic neuropathy (eg, disc hemorrhage; visible nerve fiber layer defects; notching or vertical ovalization of the cup; asymmetric cupping, especially if >0.7) are observed. Progressive cupping, even in the absence of visual field loss, can be glaucoma and should be treated as such. Otherwise, it depends on the assessment of risk factors and benefit of therapy to the patient, as to whether therapy should be initiated.
    • Discuss the pros and cons of treatment versus observation with the patient. Individualization of therapy is the key; an ideal pressure in one patient may cause glaucomatous damage in another patient. All the risk factors and systemic conditions, life expectancy of the patient, quality of life issues, and the patient's desire for therapy should be weighed when considering treatment.
    • Because of the high risk of optic nerve damage, most ophthalmologists treat if pressures are consistently higher than 28-30 mm Hg. If treatment is based on a high IOP only, then it should be ensured that the risks of treatment do not exceed the risk of the disease.
    • Other reasons to treat include such symptoms as halos, blurred vision, or pain, or recent elevation of IOP, with continuing elevation on successive visits.
    • The initiation of a monocular trial (see Medication) also may be useful in helping to decide whether to treat (ie, if the medication is effective in achieving good pressure reduction without adverse effects, that might argue in favor of treatment, instead of just observation).
    • Considering all of the above, there is still no consensus on what is the appropriate medical treatment for preventing or delaying the damage due to POAG when a patient has only elevated IOP and no other signs of POAG.[61] No one has yet been able to define conclusively which subgroups are the ones that will develop damage if left untreated, as opposed to those who will not sustain damage even if not treated.
  • Medical therapy versus observation
    • The question of medical therapy versus observation is being addressed by the OHTS, which is a multicenter, prospective, randomized, controlled, clinical trial studying more than 1600 research subjects to evaluate the safety and efficacy of medical treatment in preventing or delaying onset of visual field loss and/or optic nerve damage in patients with ocular hypertension who are at moderate risk for developing POAG.[61]
    • The OHTS medical therapy goal for the treated group is stepped therapy to reduce IOP by at least 20% from the average baseline IOP with its treated absolute value being 24 mm Hg or lower.
    • So far, the results show a 10% risk over 5 years of developing glaucoma in patients with baseline IOP of 24-31 mm Hg. This risk was reduced to 5% with medical therapy.
    • The OHTS also revealed the importance of pachymetry as a diagnostic tool and in the workup (see the images below).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).
    • Several sources agree on this initial goal of 20-25% reduction, while some specialists believe that more absolute numbers of lower than 15 should be the goal of treatment. The IOP goal must be set independently for each patient, depending on the risk factors, because an IOP level for one person with minimal risk factors may be far too high for a patient with multiple risks for sustaining glaucomatous damage.
    • Other regimens have been suggested. For minimal risk factors, consider lowering IOP by 20-30%; if a moderate number of risk factors are present, lower by 30-40%; and, in cases of numerous risk factors with markedly elevated pressures, reduction in the 40-60% range may need to be achieved to prevent neuronal loss.
    • If the patient is older than 65 years, consider treatment to keep IOP 25 mm Hg or lower, secondary to 3% risk of vascular occlusion in ocular hypertensives.
    • In any case, periodically reevaluate the target IOP, and perform regular review of IOP trends to determine whether the patient is consistently maintaining that goal.
  • The following is one suggested time guideline for therapy and follow-up testing based on initial IOP level (adjust frequency of follow-up testing as needed based on the number of risk factors and clinical picture):
    • IOP 28 mm Hg or higher: Treat patients with therapy (see Medication) and have them return in 1 month to assess if the treatment is effective and that there are no adverse effects. If the goal is reached, then perform follow-up testing every 3-4 months.
    • IOP 26-27 mm Hg: Complete follow-up testing in 2-3 weeks for rechecking pressure. If IOP is still within 3 mm of the initial reading, then continue follow-up testing every 3-4 months with visual field and dilated optic nerve evaluation at least once a year. If IOP is lower, then consider a longer time between the pressure checks, making sure to recheck IOP at different times of the day on subsequent appointments.
    • IOP 22-25 mm Hg: Perform follow-up testing 2-3 months later for recheck of IOP at different times of the day (ie, 8 am, 11 am, 1 pm, and 4 pm). If it is still within 3 mm of the initial reading at second visit, then perform follow-up testing at 6 months with Humphrey visual field testing and dilated optic nerve evaluation; repeat testing at least yearly.
  • Other caveats concerning follow-up testing include the following:
    • If a visual field defect becomes apparent on testing, confirm with repeat (possibly multiple) examinations during future office visits before using it as a basis for the treatment of presumed early POAG.
    • Perform gonioscopy at least once every 1-2 years if a significant increase in IOP occurs or if miotic therapy is instituted.
    • Repeat optic disc photos after the initial examination if a change in disc appearance is noted (or every 1-2 years if available).[62]
      • Technologic and financial barriers, as well as increasing lack of trained ophthalmic staff, are making optic disc photos more difficult to obtain in many practices.
      • Whether nerve fiber layer imaging technologies (instead of recurring, serial optic disc photos) are sufficient for mainstream nontertiary ophthalmology practices is still under debate.
    • Retinal tomography, ocular coherence tomography, and/or laser polarimetry should be measured at baseline and then every 1-2 years.[50, 63, 64] The results should be correlated with visual field results, IOP measurements, and examination findings.[65]
Next

Surgical Care

  • Generally, if control cannot be achieved with 1-2 medications, reconsider the diagnosis of ocular hypertension as possibly that of early POAG.
  • Laser and surgical therapy are not viewed to be the mainstay treatment for ocular hypertension because risks of both laser trabeculoplasty and surgery are higher than the actual risk of developing glaucomatous damage from ocular hypertension.
  • Selective laser trabeculoplasty
    • Selective laser trabeculoplasty (SLT) uses a Q-switched 532 Nd:YAG laser to selectively target pigmented cells of the trabecular meshwork in a nonthermal manner, increasing fluid outflow and thereby lowering IOP.[66, 67]
    • The 3-nanosecond high-energy specific wavelength of light used induces the same cell replacement mechanism as traditional argon laser therapy (ALT) but without the destructive burning and obliteration of structural support tissue in the meshwork.[68, 69] The short pulse of the laser does not allow time for heat to spread to other cells. SLT delivers just enough energy to the trabecular meshwork to target specific melanin-rich cells, without incurring collateral thermal damage and scarring to adjacent nonpigmented trabecular meshwork cells and underlying trabecular beams. When treated with SLT, a primarily biologic response is induced in the trabecular meshwork that involves the release of cytokines that trigger macrophage recruitment as well as other changes leading to IOP reduction.[70, 71]
    • The laser beam bypasses surrounding tissue leaving it undamaged by light. Unlike ALT, SLT can be repeated several times. Whereas patients treated with ALT can receive only 2 treatments in their lifetime, patients treated with SLT can receive 2 treatments a year.
    • SLT requires a specially designed laser, as follows:
      • A short pulse to allow for thermal relaxation
      • Precise wavelength for optimal melanin absorption
      • Sufficient energy to heat melanin to the point that it releases cytokines
      • Sufficient spot size to ensure full coverage at the trabecular meshwork
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Consultations

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

Example of progressive visual field loss over timeExample 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. Advanced glaucomatous damage with increased cuppinAdvanced glaucomatous damage with increased cupping and substantial pallor of the optic nerve head. Courtesy of M. Bruce Shields.
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Proceed to Medication
 
 
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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