Ocular Hypertension: When to Treat?

Figure

Glaucoma isthe leadingcause ofblindness inthe UnitedStates.¹Nearly 3 millionpersons have the disease,and about 100,000 newcases are diagnosed eachyear.¹ Between 3 and 6 millionAmericans are thoughtto be at increased risk forglaucoma because of elevatedintraocular pressure(IOP).²

To treat glaucoma, theIOP must be lowered by eitherpharmacologic or surgicalintervention to reduceaqueous humor productionor to increase its outflow.³Although optic nerve headand optic nerve fiber layerimaging have enhancedthe diagnosis of glaucoma,^4,5the question of whento begin treatment in a patientwith ocular hypertension(and in whom an elevatedIOP is the only signof possible glaucomatousdamage) has gone largelyunanswered.

Some practitionerspostpone therapy andmonitor patients regularly.The rationale for this approachis that withholdingtreatment spares patientsthe inconvenience of takingmedication or the risksof surgery. In addition, thepotentially serious ocularand systemic side effectsthat are associated particularlywith older agents,such as epinephrine andβ-blockers, and the financialburden of medicationcan be avoided. A recentstudy found that the costof maximum, multipledrugglaucoma therapycan consume up to 11% ofan elderly patient's annualincome.⁶

Physicians who preferto initiate treatment soonerpoint to histologic studiesof patients with ocular hypertensionwho sustained adiffuse loss of 40% of opticnerve fibers even thoughtheir visual fields remainednormal.⁷Thus, by the timeevidence of glaucoma damageis documented, significantoptic nerve fiber losshas already occurred andthe involved nerve fibersmay be even more susceptibleto damage.

AN IMPORTANTNEW STUDY
The results of the recentOcular HypertensionTreatment Study (OHTS)reassure physicians of thebenefit of early medical interventionin patients whoare at moderate to highrisk for glaucoma. Further,the results indicate thatthis approach may preventthe disease.⁸

The multicenter studyincluded 1636 patients betweenthe ages of 40 and 80years who had elevatedIOP (24 mm Hg or greaterin at least 1 eye) and noother signs of glaucoma.Their IOP was between 24and 32 mm Hg in 1 eye andbetween 21 and 32 mm Hgin the other eye. Half thegroup were randomly assignedto receive dailypressure-lowering eyedrops;the other half weregiven no medication andobserved. The IOP of themedicated patients decreasedby 22.5% 9.9%.

After 5 years, the cumulativeprobability of primaryopen-angle glaucomain those who used pressure-lowering eyedropswas reduced by 60%. Glaucomadeveloped in 36 patients(4.4%) in the medicationgroup and in 89patients (9.5%) in the observationgroup. The resultsclearly demonstrate thattreatment delays or preventsglaucomatous visualfield loss, optic nerve damage,or both. Furthermore,patients in the medicationgroup reported no adverseocular or systemic symptomsassociated with therapy;this suggests that thepressure-lowering dropsavailable today, such as selectiveα₂-adrenergic agonists,prostaglandins,prostamide analogs, andcarbonic anhydrase inhibitors,are safe and welltolerated.

WHO IS ATHIGH RISK?
Note that glaucomadeveloped in fewer than10% of the untreated patients.This raises the compellingquestion, "Whichpatients will benefit fromearly treatment?"

The authors of an analysisof OHTS confirmedthat the following factors indicatea patient is at increasedrisk for the developmentof optic disc or visualfield changes characteristicof primary open-angleglaucoma⁹:

• An elevated IOP.
• Age older than 40 years.
• Larger cup-disc ratios(Figure).
• Larger pattern standarddeviation findings on automatedcomputerized visualfield analysis. (Becauseeach patient must undergomultiple visual field testsfor the analysis, this predictivemethod may not beclinically useful in generalpractice.)
• A thin central cornea,which can cause the IOP tobe underestimated.

The OHTS did notverify earlier findings thatthose with a family historyof glaucoma are at greaterrisk.^10,11 The authors believethat population surveysand genetic studiesare more appropriate forevaluating the heritable aspectsof glaucoma.

Other studies havefound that glaucoma ismore prevalent amongAfrican Americans thanamong white persons.^12,13When the thinner centralcorneal measurements andlarger baseline cup-discratios of black OHTS participantswere evaluatedunder multivariate analysisthat adjusted for these factors,race was no longer astatistically significantpredictor.

PATIENT EDUCATIONSTILL KEY
During counseling, explainthe patient's risk factorsfor glaucoma in thecontext of his or her healthstatus and life expectancy.Discuss the possible sideeffects, inconvenience, andcost of daily treatment-along with the benefits reportedin OHTS.

Some patients willnot want treatment unlessit is absolutely necessary.For those at low risk, a reasonableplan is to monitorthe patient carefully and intervenewhen the first signof damage is noted. However,for those with multiplerisk factors, it is prudentto initiate medical therapyearly.

References:

REFERENCES:1. Young P. Glaucoma and Neurodegeneration.New York: Research toPrevent Blindness; 2001.
2. Lebowitz HM, Krueger DE,Maunder LR, et al. The FraminghamEye Study monograph: an ophthalmologicaland epidemiologicalstudy of cataract, glaucoma, diabeticretinopathy, macular degeneration,and visual acuity in a generalpopulation of 2631 adults, 1973-1975.Surv Ophthalmol. 1980;24(suppl):335-610.
3. Bartlett JD, Jaanus SD, Fiscella RG,Sharir M. Ocular hypotensive drugs.In: Bartlett JD, Jaanus SD, Blaho KE,et al, eds. Clinical Ocular Pharmacology.4th ed. Boston: Butterworth-Heinemann;2001:167-218.
4. Johnson CA. Psychophysical measurementof glaucomatous damage.Surv Ophthalmol. 2001;45(suppl 3):S313-S318.
5. Zangwill LM, Chang CF, WilliamsJM, Weinreb RN. New technologiesfor diagnosing and monitoring glaucomatousoptic neuropathy. OptomVis Sci. 1999;76:526-536.
6. Doyle JW, Smith MF, Tierney JWJr. Glaucoma medical treatment-2002: does yearly cost now equal theyear? Optom Vis Sci. 2002;79:489-492.
7. Quigley HA, Addicks EM, GreenWR. Optic nerve damage in humanglaucoma, III: quantitative correlationof nerve fiber loss and visual field defectin glaucoma, ischemic neuropathy,papilledema, and toxic neuropathy.Arch Ophthalmol. 1982;100:135-146.
8. Kass MA, Heuer DK, HigginbothamEJ, et al, for the Ocular HypertensionTreatment Study. A randomizedtrial determines that topical ocular hypotensivemedication delays or preventsthe onset of primary open-angleglaucoma. Arch Ophthalmol. 2002;120:701-713.
9. Gordon MO, Beiser JA, Brandt JD,et al, for the Ocular HypertensionTreatment Study. Baseline factors thatpredict the onset of primary openangleglaucoma. Arch Ophthalmol.2002;120:714-720.
10. Tielsch JM, Katz J, Sommer A,et al, for the Baltimore Eye Survey.Family history and risk of primaryopen-angle glaucoma. Arch Ophthalmol.1994;12:69-73.
11. Leske MC, Nemesure B, He Q,et al. Patterns of open-angle glaucomain the Barbados Family Study.Ophthalmology. 2001;108:1015-1022.
12. Tielsch JM, Sommer A, Katz J, etal, for the Baltimore Eye Survey.Racial variations in the prevalence ofprimary open-angle glaucoma. JAMA.1991;266:369-374.
13. Turner CC. Open-angle glaucoma:a survey of racial incidence. Am JOptom Physiol Opt. 1967;44:56-57.