eMedicine Specialties > Ophthalmology > Intraocular Pressure

Ocular Hypertension: Treatment & Medication

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

Treatment

Medical Care

Some controversy still exists about when to treat ocular hypertension. 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. 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.

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. 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.

  • Several questions should be asked when considering treatment: Is the elevated pressure significant? Will this patient develop visual loss if left untreated? 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. 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.
    • 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 Media files 10-11). 
    • 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).
      • 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. The results should be correlated with visual field results, IOP measurements, and examination findings.

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.
    • 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. 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.
    • 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

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.

Medication

The ideal drug for treatment of ocular hypertension should have the following characteristics: (1) effectively lower IOP, (2) no adverse effects or systemic exacerbation of disease, and (3) inexpensive with once-a-day dosing. However, because no medicine possesses all of the above, these qualities must be prioritized based on the patient's individual needs and risks; then, therapy should be chosen accordingly.

Older glaucoma medications, such as cholinergics (ie, miotics, such as pilocarpine) and osmotics, as well as nonselective adrenergic agonists, have a limited role in the treatment of ocular hypertension and should only be considered if adverse effects prevent the use of the above-described medications.

Newer products having possible neuroprotective effects (eg, memantine, which is an N-methyl-D-aspartate [NMDA] receptor antagonist), as well as new multiple-agent combinations, are likely to be available in the future. Their role in the treatment of ocular hypertension will have to be studied as they become available for use.

Once a medication has been initiated, perform close follow-up care to assess its effect. Perform initial follow-up care 3-4 weeks after the beginning of therapy. Recheck IOP at the drug's peak and trough times to see if target IOP has been reached and is maintained throughout the day. Observe for signs of allergy to the medication (eg, hyperemia, skin rash, follicular reaction). Query patients about the presence of any systemic adverse effects and symptoms. Continue the treatment if a therapeutic trial has shown effective lowering of IOP without adverse effects. Reevaluate 2-4 months later, depending on the clinical picture.

Consider a monocular therapeutic trial when first initiating the medical therapy, since IOP in the other eye can be used as a baseline control to gauge effect of a medication (particularly useful in patients with a widely fluctuating diurnal curve). A difference of more than 4 mm Hg between the 2 eyes after treatment is strongly suggestive of a clinical effect. However, some agents (especially beta-blockers) may have crossover effects on the other eye even with monocular treatment, and so clinical correlation must be kept in mind. If monocular therapy is found to be effective, consider initiating binocular therapy.

Some medications (eg, latanoprost, brimonidine) may have an effect that plateaus at 6-8 weeks in certain patients; keep this in mind when scheduling further follow-up examinations. Other patients will be nonresponders to some therapies. If this occurs, discontinue the medication and initiate a new drug. While discontinuing or changing therapies, keep in mind that many drugs have a wash-out period of up to 2-4 weeks (especially beta-blockers), during which they may still have some IOP-lowering effect or residual systemic response.

If one medication is not adequate in reaching the target pressure, choose a second medication that has a different mechanism of action, so that the 2 drug therapies will have an additive effect. (Usually, no additive effect is seen if 2 medications from the same drug class are used.)

Administer a specific plan of pharmacotherapy only after the possible effects of the systemic medications (eg, beta-blockers, calcium channel blockers, ACE inhibitors) that a patient is taking have been taken into consideration.

See AAO's Ophthalmology monograph #13 for an in-depth description of particular drugs.

Carbonic anhydrase inhibitors (CAIs)

By slowing the formation of bicarbonate ions with subsequent reduction in sodium and fluid transport, it may inhibit carbonic anhydrase (CA) in the ciliary processes of the eye. This effect decreases aqueous humor secretion, reducing IOP. These agents typically have a weaker effect than beta-blockers. The more commonly used drug of this type for the treatment of ocular hypertension is in the combination medication Cosopt (which may be tried if single agent beta-blocker therapy has had suboptimal results).


Dorzolamide (Trusopt)

Reversible carbonic anhydrase inhibitor that may decrease aqueous humor secretion, causing a decrease in IOP. Presumably, it slows bicarbonate ion formation with subsequent reduction in sodium and fluid transport.
Systemic absorption can affect carbonic anhydrase in the kidney, reducing hydrogen ion secretion at renal tubule, and increasing renal excretion of sodium, potassium bicarbonate, and water.
Less stinging on instillation, secondary to buffered pH.

Adult

1 gtt in affected eye(s) bid/tid; usually tid if using as a single agent, bid if used in conjunction with other agents

Pediatric

Not established

Coadministration with high-dose salicylate therapy may increase toxicity; may have additive systemic effects if patient is already on oral CAIs

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Local ocular adverse effects, primarily conjunctivitis and lid reactions, may occur with long-term administration of dorzolamide (discontinue therapy and evaluate patient before restarting therapy); oral dosage form can cause paresthesias, malaise, anorexia, and poor tolerance of carbonated beverages; there is rare incidence of aplastic anemia associated with its use (baseline CBC and at least 1 follow-up CBC should be considered in the first 6 mo of treatment to monitor therapy)


Brinzolamide (Azopt)

Catalyzes reversible reaction involving hydration of carbon dioxide and dehydration of carbonic acid. May use concomitantly with other topical ophthalmic drug products to lower IOP. If more than 1 topical ophthalmic drug is being used, administer drugs at least 10 min apart.

Adult

1 gtt in affected eye(s) tid

Pediatric

Not established

May have additive systemic effects if patient is already on oral CAIs

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Local ocular adverse effects, primarily conjunctivitis and lid reactions, may occur with long-term administration (discontinue therapy and evaluate patient before restarting therapy)


Acetazolamide (Diamox, Diamox Sequels)

Primarily used only for the treatment of refractory POAG and secondary glaucomas. Because of increased incidence of adverse effects, rarely indicated for treatment of ocular hypertension.

Adult

Tablets: 125-250 mg PO qid
Sequels: 500 mg PO bid

Pediatric

Not established; suggested dose is as in adults

Can decrease therapeutic levels of lithium and alter excretion of drugs (amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine

Documented hypersensitivity; hepatic disease; severe renal disease; adrenocortical insufficiency; severe pulmonary obstruction

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Patients with impaired hepatic function may go into coma; may cause substantial increase in blood glucose in some diabetic patients


Timolol/dorzolamide (Cosopt)

Carbonic anhydrase inhibitor that may decrease aqueous humor secretion, causing a decrease in IOP. Presumably slows bicarbonate ion formation with subsequent reduction in sodium and fluid transport.
Timolol is a nonselective beta-adrenergic receptor blocker that decreases IOP by decreasing aqueous humor secretion and may slightly increase outflow facility.
Both agents administered together bid may result in additional IOP reduction compared with either component administered alone, but reduction is not as much as when dorzolamide tid and timolol bid are administered concomitantly.

Adult

1 gtt in affected eye(s) bid

Pediatric

Not established

Coadministration with high-dose salicylate therapy may increase toxicity; may have additive systemic effects if patient is already on oral CAIs

Documented hypersensitivity; COPD; CHF; asthma; cardiac conduction defects; breastfeeding

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Local ocular adverse effects, primarily conjunctivitis and lid reactions, may occur with chronic administration of dorzolamide (discontinue therapy and evaluate patient before restarting therapy); product may have sulfites, which may cause allergic-type reactions in susceptible patients


Methazolamide (Neptazane)

Reduces aqueous humor formation by inhibiting enzyme carbonic anhydrase, which results in decreased IOP.

Adult

25-50 mg PO bid/tid initially; not to exceed 150 mg PO bid

Pediatric

Not established

May increase toxicity of salicylate, digoxin; coadministration with other diuretics may induce hypokalemia; decreases effects of lithium and alter excretion of other drugs by alkalinizing urine

Documented hypersensitivity; renal impairment

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in respiratory acidosis and diabetes mellitus; impairs mental alertness and/or physical coordination; hematuria, glycosuria, polyuria, hepatic insufficiency, bone marrow suppression, thrombocytopenia/purpura, agranulocytosis, urticaria, pruritus, and rash may occur

Adrenergic agonists

Of this class, the alpha2-selective agonist, brimonidine, is the most commonly used for the treatment of ocular hypertension. Apraclonidine is an alpha2-selective agonist but is believed to have more of an allergic potential, so it rarely is used as a long-term medication. Less selective adrenergics, such as epinephrine and dipivefrin, also can have a significantly higher allergic component and other substantial adverse effects, such as exacerbation of hypertension, angina, palpitations, or cystoid macular edema (CME). Because these less selective agents are used infrequently in treating ocular hypertension, they are not discussed herein. Alpha2-adrenergic agonists work by decreasing aqueous production.


Brimonidine (Alphagan, Alphagan-P)

Relatively selective alpha2-adrenergic receptor agonist, decreases IOP by dual mechanisms. Reduces aqueous humor production and increases uveoscleral outflow. Has minimal effect on cardiovascular and pulmonary parameters. A moderate risk of allergic response to this drug exists. Caution should be used in individuals who have developed an allergy to Iopidine. IOP lowering of up to 27% reported.
The brand Alphagan-P contains the preservative Purite and has been shown to be much better tolerated than its counterpart Alphagan.

Adult

1 gtt in affected eye(s) bid/tid; a bid frequency is used initially, especially if in combination with other classes of agents; in single-agent therapy, tid dosing is used most often when bid frequency does not adequately control IOP

Pediatric

Not established

Coadministration with topical beta-blockers may further decrease IOP; tricyclic antidepressants may decrease effects of brimonidine; CNS depressants, such as barbiturates, opiates, and sedatives, may potentiate effects of brimonidine

Documented hypersensitivity; patients receiving MAOIs

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May exacerbate or precipitate ocular irritation, topical sensitivity, vasovagal attack, and optic nerve ischemia in patients with advanced glaucomatous optic neuropathy; caution if patient is aphakic, pseudophakic, or has history of CME or allergic response to Iopidine; systemic adverse effects include dry mouth, fatigue, drowsiness, allergic (follicular) conjunctivitis, contact dermatitis


Apraclonidine 0.5%, 1% (Iopidine)

Potent alpha-adrenergic agent selective for alpha2-receptors with minimal cross-reactivity to alpha1-receptors. Suppresses aqueous production. Reduces elevated, as well as normal, intraocular pressure (IOP) whether accompanied by glaucoma or not. Apraclonidine is relatively selective alpha-adrenergic agonist that does not have significant local anesthetic activity. Has minimal cardiovascular effects.

Adult

1 gtt of 0.5% or 1% in affected eye(s) tid

Pediatric

Not established

Monitor pulse and BP frequently when giving cardiovascular drugs; not for use concurrently with MAO inhibitors

Documented hypersensitivity; patients on MAO inhibitors or have taken them in the past 14 d

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May exacerbate or precipitate ocular irritation, topical sensitivity, vasovagal attack and optic nerve ischemia in patients with advanced glaucomatous optic neuropathy

Prostaglandin analogs

Newer class of medication that works by increasing uveoscleral outflow.

Unoprostone (Rescula), bimatoprost (Lumigan), and travoprost (Travatan) are examples of newly approved drug analogues similar to prostaglandins that may help in IOP reduction. All 3 of these drugs are new alternatives in the armamentarium of medications to treat elevated IOP. Limited data are available on these drugs, but each has its own set of characteristics that may be useful in the clinical setting. Unoprostone has been shown to decrease pressure approximately 10-15% and may work partially through traditional outflow channels. Bimatoprost may achieve a large reduction in pressure in many patients but has been known to cause significant conjunctival hyperemia. Travoprost has been purported to achieve lower IOPs, particularly in patients of African American descent, but these data are in doubt and the subject of controversy. It also may cause significant conjunctival hyperemia.


Latanoprost (Xalatan 0.005%)

May decrease IOP by increasing outflow of aqueous humor. Patients should be informed on possible cosmetic effects to eye/eyelashes, especially if uniocular therapy is to be initiated.

Adult

1 gtt in affected eye(s) qhs

Pediatric

Not established

Coadministration with eye drops containing the preservative thimerosal may reduce effects (administer at intervals of 5 min between applications); effect may be additive if used with miotic agents (eg, pilocarpine), which decrease uveoscleral outflow

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Patients who are pregnant or breastfeeding should use caution because knowledge of effects on pediatric patients is limited; caution in history of uveitis or CME and monocular therapy because lash and iris color changes may occur; increased pigmentation of iris and eyelashes; increased growth (hypertrichosis) of eyelashes and adjacent hair; conjunctival hyperemia; may promote baseline intraocular inflammation


Bimatoprost ophthalmic solution (Lumigan)

A prostamide analogue with ocular hypotensive activity. Mimics the IOP-lowering activity of prostamides via the prostamide pathway. Used to reduce IOP in open-angle glaucoma or ocular hypertension.

Adult

1 gtt of 0.03% solution in affected eye(s) hs; not to exceed 1 dose/d

Pediatric

Not established

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause permanent increase in pigment to iris (ie, increases brown pigment) and eyelid; may increase eyelash growth; may cause bacterial keratitis; caution in uveitis or macular edema; do not instill if wearing contact lenses


Travoprost ophthalmic solution (Travatan)

Prostaglandin F2-alpha analog. Selective FP prostanoid receptor agonist believed to reduce IOP by increasing uveoscleral outflow. Used to treat open-angle glaucoma or ocular hypertension.

Adult

1 gtt in affected eye(s) hs; not to exceed 1 dose/d

Pediatric

Not established

Documented hypersensitivity; pregnancy

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Commonly causes ocular hyperemia; may cause permanent increase in pigment to iris (ie, increases brown pigment) and eyelid; may increase eyelash growth; may cause bacterial keratitis; caution in uveitis or macular edema; do not instill if wearing contact lenses


Unoprostone ophthalmic solution (Rescula)

Prostaglandin F2-alpha analog. Selective FP prostanoid receptor agonist believed to reduce IOP by increasing uveoscleral outflow. Used to treat open-angle glaucoma or ocular hypertension.

Adult

1 gtt in affected eye(s) bid

Pediatric

Not established

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Commonly causes ocular hyperemia; may cause permanent increase in pigment to iris (ie, increases brown pigment) and eyelid; may increase eyelash growth; may cause bacterial keratitis; caution in uveitis or macular edema; do not instill if wearing contact lenses

Beta-adrenergic blockers

Decreases aqueous production, possibly by blocking adrenergic beta-receptors present in the ciliary body. Unfortunately, the nonselective medications in this class also interact with the beta-receptors in the heart and lungs, causing significant adverse effects.


Betaxolol 0.25% (Betoptic-S)

Levobetaxolol (Betaxon) -- Selectively blocks beta1-adrenergic receptors with little or no effect on beta2-receptors. Reduces IOP by reducing production of aqueous humor. May have less pulmonary effects. IOP-lowering effect is slightly less than nonselective beta-blockers. May increase optic nerve perfusion and confer neuroprotection.

Adult

1 gtt in affected eye(s) bid

Pediatric

Not established

May have additive systemic effects if patient is already on systemic beta-blockers

Documented hypersensitivity; bronchial asthma; severe COPD; sinus bradycardia; second- and third-degree AV block; overt cardiac failure; cardiogenic shock

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Product may have sulfites, which may cause allergic-type reactions in susceptible patients; may exacerbate or precipitate heart block, asthma, COPD, and mental changes (especially in elderly patients); may cause blurred vision and eye ache; should be avoided in women who are breastfeeding because beta-blockers can be found concentrated in breast milk


Carteolol 1% (Ocupress)

Has an intrinsic sympathomimetic activity (partial agonist activity), with possibly less cardiac and lipid profile adverse effects.

Adult

1 gtt in affected eye(s) bid

Pediatric

Not established

May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)

Documented hypersensitivity; bronchial asthma; sinus bradycardia; second- and third-degree AV block; severe COPD; overt cardiac failure; cardiogenic shock

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Product may have sulfites, which may cause allergic-type reactions in susceptible patients; may exacerbate or precipitate heart block, asthma, COPD, and mental changes especially in elderly patients); may cause blurred vision and eye ache; should be avoided in women who are breastfeeding because beta-blockers can be found concentrated in breast milk


Timolol 0.25%, 0.5% (Timoptic, Timoptic XE, Blocadren, Istalol)

May reduce elevated and normal IOP, with or without glaucoma by reducing production of aqueous humor. Timolol gel-forming solution (Timoptic XE) usually is administered at night, unless used concurrently with latanoprost therapy.
The brands Timoptic XE and Istalol are both administered qd. However, Timoptic XE is a gel-forming solution, while Istalol is an aqueous solution.

Adult

Timolol: 1 gtt in affected eye(s) bid
Timolol XE: 1 gtt in affected eye(s) qd

Pediatric

Not established

May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)

Documented hypersensitivity; bronchial asthma; sinus bradycardia; second- and third-degree AV block; severe COPD; overt cardiac failure; cardiogenic shock

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Product may have sulfites, which may cause allergic-type reactions in susceptible patients; may exacerbate or precipitate heart block, asthma, COPD, and mental changes (especially in elderly patients); may cause blurred vision and eye ache; should be avoided in women who are breastfeeding because beta-blockers can be found concentrated in breast milk


Levobunolol 0.25%, 0.5% (Betagan, AKBeta)

Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production and possibly increasing outflow of aqueous humor.

Adult

1 gtt in affected eye(s) bid

Pediatric

Not established

May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)

Documented hypersensitivity; bronchial asthma; severe COPD; sinus bradycardia; second- and third-degree AV block; overt cardiac failure; cardiogenic shock

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Product may have sulfites, which may cause allergic-type reactions in susceptible patients; may exacerbate or precipitate heart block, asthma, COPD, and mental changes (especially in elderly patients); may cause blurred vision and eye ache; should be avoided in women who are breastfeeding because beta-blockers can be found concentrated in breast milk


Metipranolol 0.3% (OptiPranolol)

Beta-adrenergic blocker that has little or no intrinsic sympathomimetic effects and membrane-stabilizing activity. Has little local anesthetic activity. Reduces IOP by reducing production of aqueous humor.

Adult

1 gtt in affected eye(s) bid

Pediatric

Not established

May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)

Documented hypersensitivity; sinus tachycardia; cardiac failure; cardiogenic shock; second- and third-degree AV block

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Product may have sulfites, which may cause allergic-type reactions in susceptible patients; may exacerbate or precipitate heart block, asthma, COPD, and mental changes (especially in elderly patients); may cause blurred vision and eye ache; should be avoided in women who are breastfeeding because beta-blockers can be found concentrated in breast milk

Less-selective sympathomimetics

These less-selective adrenergic drugs increase outflow of aqueous humor through the trabecular meshwork and possibly through the uveoscleral outflow pathway, probably by a beta2-agonist action. Up to one third of patients will not respond to these drugs.

Less-selective adrenergics, such as epinephrine, dipivefrin, and memantine also can have a significantly higher allergic component and other substantial adverse effects, such as exacerbation of hypertension, angina, palpitations, or cystoid macular edema (CME). These less-selective agents are used infrequently. Memantine, increases outflow of aqueous humor through the trabecular meshwork and possibly through the uveoscleral outflow pathway, probably by a beta2-agonist action.


Epinephrine 0.5%, 1%, 2% (Epifrin)

Lowers IOP by increasing outflow and reducing production of aqueous humor. Used as adjunct to miotic or beta-blocker therapy. Combination of miotic and sympathomimetic will have additive effects in lowering IOP.

Adult

1 gtt in affected eye(s) qd/bid

Pediatric

Not established

Increases toxicity of beta- and alpha-blocking agents

Documented hypersensitivity; narrow- or shallow-angle glaucoma; aphakia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in cardiac arrhythmias


Dipivefrin (AKPro, Propine)

Prodrug converted to epinephrine in eye by enzymatic hydrolysis. Appears to act by decreasing aqueous production and enhancing outflow facility. Has same therapeutic effect as epinephrine with fewer local and systemic adverse effects. May be used as an initial therapy or as an adjunct with other antiglaucoma agents for the control of IOP.

Adult

1 gtt in affected eye(s) bid

Pediatric

Not established

Increased or synergistic effects are seen when used concurrently with agents that lower intraocular pressure

Documented hypersensitivity; narrow-angles; dilation of pupil may predispose patient to attack of angle-closure glaucoma

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Macular edema occurs in up to 30% of aphakic patients treated with epinephrine; discontinuation of treatment generally results in reversal of maculopathy; caution in vascular hypertension


Memantine (Namenda, Axura)

Indicated for moderate-to-severe Alzheimer disease; currently still in Phase 3 trial for possible neuroprotective systemic treatment of glaucoma, although as of now, this is a non-FDA approved off-label use of the drug. N-methyl-D-aspartate (NMDA) antagonist. NMDA receptor stimulation in the CNS by glutamate (an excitatory amino acid) is hypothesized to contribute to Alzheimer symptoms, as well as apoptosis (programmed cell death) and neuronal degeneration.

Adult

5 mg PO qd initially; gradually titrate to a target dose of 20 mg/d using the following dosage regimen (allow at least 1-2 wk between each dosage increase, particularly if side effects, such as headache or nausea, occur): 5 mg PO bid; then, 5 mg PO qam and 10 mg PO qpm; then, 10 mg PO bid

Pediatric

Not indicated

Coadministration with drugs causing alkaline urine (eg, sodium bicarbonate, carbonic anhydrase inhibitors) may decrease clearance by 80%, thus accumulation and toxicity may occur (eg, caution should be used in patients also on acetazolamide [Diamox] or other carbonic anhydrase inhibitors, although memantine has been used clinically with acetazolamide without morbidity when patients are monitored appropriately and dosages adjusted); coadministration with other NMDA antagonists (eg, amantadine, ketamine, dextromethorphan) may increase toxicity risk; concurrent use with other drugs renally eliminated via tubular secretion (eg, hydrochlorothiazide, triamterene, cimetidine, ranitidine, quinidine, nicotine) may alter plasma levels of either drug

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Common adverse effects include dizziness (7%), headache (6%), and constipation (5%); predominantly excreted renally, no data support use with severe renal impairment

Beta-blocker / Alpha Agonist Combination

Combination solution may further decrease aqueous humor secretion compared to each solution used as monotherapy, while improving compliance.


Brimonidine/timolol (Combigan)

Selective alpha-2 adrenergic receptor agonist with a nonselective beta-adrenergic receptor inhibitor. Each of them decrease elevated IOP, whether or not associated with glaucoma.

Adult

1 gtt in affected eye(s) bid approximately q12h

Pediatric

Not established

May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects); coadministration with topical beta-blockers may further decrease IOP; tricyclic antidepressants may decrease effects of brimonidine; CNS depressants (eg, barbiturates, opiates, sedatives) may potentiate effects of brimonidine

Documented hypersensitivity; bronchial asthma; sinus bradycardia; second- and third-degree AV block; severe chronic obstructive pulmonary disease; overt cardiac failure; cardiogenic shock; patients receiving MAOIs

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Beta-blockade may potentiate muscle weakness that is consistent with certain myasthenic symptoms (eg, diplopia, ptosis, generalized weakness); product may have sulfites, which may cause allergic-type reactions in certain susceptible persons; caution in cardiovascular disease, depression, cerebral or coronary insufficiency, orthostatic hypotension, and Raynaud syndrome; punctal occlusion may help minimize adverse effects; caution if patient is aphakic, pseudophakic, or has history of CME or allergic response to Iopidine

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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