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tommon Eye Diseases of Elderly People:Identifying and Treating Causes of

fision LossW",

I~tricia T. Harvey

Isian Science Research Programme, Toronto Western Hospital, Toronto, Canada,*'

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Ige-related macular degeneration. Cataract.I>iabeticretinopathy. Glaucoma. Verteporfintherapy19,

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bstract

fthe38 million people who are blind, the majority, 22iTlion,are 60 years of age or older. The most common

.~"ses of vision loss In elde"v people ace age-celatedtracular degeneration (AMD), cataract, glaucoma, and~iabetic retinopathy. Of these, AMD is the leading cause~.

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registered blindness in people over the age of 50 yearsp the western world. However, until recently, the treat-~ent options for people with AMD have been severely[mited. Verteporfin therapy is a new treatment that is~,fficaciousand safe in selected patients with AMD whoIre at high risk of central vision loss. Physicians who arer regular contact with elderly people can help to mini-pile vision loss in this group of patients by being alert tope symptoms and signs of age-related eye diseases.~his paper reviews each of the common eye diseases,!\lith.an emphasis on AMD because of the recent ad-~nces in treatment.

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Gerontology 2003;49: 1-11001: 10.1159/000066507

Copyright@2003S.KargerAG.Basel

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'3X+41 61 306 1234

~Mail karger@karger.ch""Y, karger.com

Accessible online at:

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Introduction

Of the 38 million people who are blind worldwide [1],22 million are over the age of 60 years (World HealthOrganization 1994 estimate). Even more people.'(110 mil-lion) suffer from low vision. These factors, combined withan increase in life expectancy [2], highlight the need foreffective eye care for elderly people to minimize visionloss from age-related conditions such as age-related macu-lar degeneration (AMD), cataract, glaucoma, and diabeticretinopathy. Vision loss is only one aspect of the impactthat these eye diseases have on the person and is frequent-ly accompanied by a corresponding decrease in their abili-ty to carry out activities of daily living and an increasedrisk of depression [3]. These aspects, which are oftenundervalued [4], may compromise an elderly person'sability to live independently.

Early diagnosis and prompt referral of patients witheye disease are important to try to maximize treatmentbenefits. When primary care physicians or primary healthcare professionals are aware of both the clinical signs andsymptoms and the treatment options that are available forthe common age-related eye diseases, they can facilitatethe improvement of these conditions in their patients. Inthis article, the diagnosis and treatment options for the

Dr. PatricIa T HarveyMed-West Medical Centre750 Dundas St. WooSte, B09

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Gerontoiogy 2003:49: i-Ii~ Harvey

common age-related eye diseases are reviewed, with anemphasis on AMD because of recent advances in treat-ment.

Age-Related Macular Degeneration

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AMD is the most common cause of severe vision loss

in people over 50 years of age in the western world [5]. It isa degenerative disorder of the retinal macula (fig. 1) thatresults in loss of central vision. AMD is classified into two

~types: non-neovascular (also known as non-exudative oratrophic AMD) and neovascular (also known as exudativeor serous AMD).

Non-neovascular AMD accounts for approximately80% of all AMD and is associated with the formation ofdrusen [6]. These are localized deposits of extracellularmaterial that often can be seen with direct dilated oph-thalmoscopy as yellow deposits in the center of the retina(fig. 2). More than 50% of people over 70 years of age'have drusen [5]; however, drusen cannot be taken as anabsolute indication of AMD. Almost all cases of severevision loss in non-neovascular AMD result from geo-graphic atrophy. Atrophy of the retinal pigment epithe-lium (RPE) is thought to be followed by loss of macularphotoreceptors and of the blood supply to the RPE, creat-ing blind spots. Neovascular AMD accounts for onlyabout 20% of all AMD, but is responsible for 90% of casesof severe, irreversible central vision loss [6].

Progression from non-neovascular AMD to neovascu-lar AMD occurs in approximately 10-20% of people withAMD [6]. The time period for the transition from non-neovascular to neovascular AMD is variable, rangingfrom a few months to several years. Neovascular AMD ischaracterized by choroidal neovascularization (CNV), theformation of new, fragile blood vessels growing from thechoroid into the sub retinal and pigment epithelial space(fig. I). These vessels leak blood and fluid, resulting inscarring, which can reduce visual acuity.

Fluorescein angiography is the most frequently usedmethod to visualize choroidal neovascular lesions. This

technique can be used to classify the lesion according toits anatomical location in the macula: subfoveal (directly

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Fig. 1. Anatomy of the eye (a) and the macula (b), with a cross-section showing damage resulting from AMD (c). Reproduced withpermission from Novartis Ophthalmics AG.

Common Eye Diseases of Elderly People

Fig. 2. Color fundus photographs showing the appearance of (a) anormal healthy retina (Image obtained from National Eye Institute,National Institutes of Health), (b) AMD with drusen (arrows) (Re-

, produced with permission from Wilmer Photograph Reading Cen-ter), (c) diabetic retinopathy with ,macular edema (arrows) (Im-age obtained from National Eye Institute, National Institutes ofHealth).

Gerontology 1003:49: I-II~

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Table 1. Symptoms and signs of age-related eye diseases

Symptoms OphthalmoscopyVisual Acuity Decrease

AMD Non-neovascular:blurred or distortedvision, central scotomaNeovascular:central scotoma, imagedistortion, increased glare sensitivity,decreased color perception, photopsias,formed hallucinations, blindness

Decreased visual acuity, clouding ofthe visual field, double vision, near-sightedness, decreased color perception,reduced contrast sensitivity, increasedglare sensitivity, blindness

CataractI!'

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Noll-neovasclllar: slow decline or

no changeNeovascular: rapid, steady decreasein visual acuity

Variable, depending on the extentand progression of glaucoma;visual acuity can stabilize withouttreatment

Non-neovascular:drusen, atrophy (the RPE (visible as alternating arecdepigmentation and hyperpigmentNeovasclllar:drusen (especiallyiftlare numerous (>20), soft, large (>6or con~uent) .

An opacity or clouding of the lens; I

be a small local opacity or a diffusegeneral loss of transparency; for antor posterior cataract, black, branchiopacities are visible

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Glaucoma Open-angle glaucoma: optic nervecupping'

Early stages are asymptomatic. In thelater stages - headaches or blurredvision after vigorous exercise, headachesaccompanied by misty vision or haloeswhen reading in low illumination,reduced visual field, blurred vision,blindness

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Slow,progressive decrease in open-angle glaucoma; can be very rapidin angle-closureglaucoma

Diabeticretinopathy

Nonproliferative:asymptomaticProliferative:blurred vision, floaters,loss of central vision, decreased colorperception, poor night vision,blindness

No decrease until qisease progressesto the proliferative'\stagewhen visualacuity loss can be rapid

N onproliferative:microaneurysms,intraretinal hemorrhages, soft exudahard exudates, venous looping, venobeading, rpacular edema, dilatedretinal veinsProliferative:proliferating endotheli1cell tubules, vascular fibrosis, intra-or peri-retinal hergorrhage, vitreoushemorrhage

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beneath the foveal avascular zone (FAZ)), juxtafoveal(1-199 11m from the center of the FAZ), or extrafoveal(2: 200 11mfrom the center of the FAZ). The visual prog-nosis is worst for subfoveallesions; approximately 60% ofCNV associated with AMD is subfoveal [7]. Fluoresceinangiography can also be used to classify the pattern of flu-orescence from CNV as classic, occult, or a mixture ofboth depending on its appearance. The development ofclassic CNV is associated with a trend toward an in-

creased risk of vision loss within a year [8]. If all thesefactors are combined, it seems that the worst visual prog-nosis in AMD occurs in patients who have neovascularlesions that are subfoveal with a large classic component.

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Ii, Signsand SymptomsPatients with non-neovascular AMD may experience

slow, progressive loss of central visual function, which ismost noticeable during tasks that require near vision,especially in the early stages of the disease [9]. Also, geo-

4 Gerontology 2003:49: I-II ""

graphic atrophy may cause blurred or distorted visiocontrast, neovascular AMD can cause a rapid detertion of central vision: approximately 70% of eyessub foveal CNV have a visual acuity of 20/200 withyears of diagnosis [10]. Furthermore, once CNVdeveloped in one eye, there is a significant risk thatsecond eye will develop CNV [11].

A decrease in central vision and a blind spot (scotoin the visual field (fig. 3) are consequences of bleedingscarring from CNV (table 1). In addition, a patient,neovascular AMD may experience image distortion (tamorphopsia). For example, they may repOli that]mally straight lines, such as pillars or fence posts, apI'wavy' or 'bent'. The patient may also report increaglare sensitivity, decreased color vision, sensationflashing or sparking lights (photopsias), and formed ha

cinations [12]..Contrast sensitivity (the ability to differtiate between an object and its background) may alsoreduced in patients with neovascular AMD [13].

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"Fig. 3. A market scene as seen by a person

~with (a) a healthy eye, (b) AMD, (c) cataract,I(d) advanced glaucoma, (e) diabetic reti-nopathy, Reproduced with permission fromtNovartis Ophthalmics AG.~

endothelial'sis, intra-:, vitreous

.ted vision, IUi Vision loss resulting from AMD has a considerablepid deterior~'\impact on the patient's ability to undertake daily activi-of eyes wit!~ties,especially if both eyes are affected [11]. The ability to

'200 within iiread, recognize common household objects, and distin-ce CNV har;guishamong facial expressions are-all affected [14]. Fur-risk that th~thermore, the vision loss associated with AMD means

::that patients have a greater risk of falls and hip fractureJot (scotomai[ 15, 16]. These factors contribute to the decrease in a per-'bleeding anc'son's quality of life. However, it appears that clinicianspatient witEimayunderestimate the effect that AMD has on the indi-

stortion (mo vidual [4].,ort that nof" Several factors may delay a diagnosis of AMD. Despiteposts, appeaHthe prevalence of AMD and its potential impact onJrt increased'patients, awareness of neovascular AMD is not as wide-sensation o!yspreadas it is for other eye diseases such as cataract or'armed hall IFglaucoma - in a survey conducted in 1999,70% of adultsy to differeD'had not heard of AMD [17], Also, elderly people often domay also bl~ot report the symptoms of vision loss [18]; they may13]. Ignore them, thinking their symptoms are a normal part of

-Common Eye Diseases of Elderly People

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aging, or they may believe nothing can be done to help[19]. Alternatively, older people may assume that symp-toms of AMD are due to the progression of cataracts, Tohelp overcome these obstacles to early diagnosis, elderlypeople should be encouraged to have eye examinationsevery 1-2 years, even in the absence of symptoms (Ameri-can Academy of Ophthalmology Policy Statement,1990),

Who Is Most at Risk of AMD?The single greatest risk factor for AMD is increasing

age, although a number of other risk factors have beensuggested. People who have neovascular AMD in one eyeshould be monitored very carefully because, over as-yearperiod, approximately 42 % of patients will develop thedisease bilaterally [11]. Studies have found that the preva-lence of AMD is associated with gender (women are morelikely to have AMD than men), race (lower prevalence inAfro-Caribbean American and Hispanic people than Cau-

Gerontology 2003:49: 1-[1~

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Fig. 4. When fixating on the center of an Amsler grid, a patient withneovascular AMD may perceive distortions or discoloration of thegrid.

casian people), and cigarette smoking [20,21]. Family his-tory also suggests genetic factors are involved [22]. Otherpossible risk factors that have been identified include car-diovascular disease, elevated serum cholesterol levels,and hypertension [11].

Studies suggest that vitamin [23] and mineral [24] sup-plements may contribute to a reduction in the risk ofdeveloping a degenerative eye disease such as AMD.Antioxidant supplements may prevent cellular damage inthe retina by reacting with, and thereby removing, freeradicals produced in the process of light absorption [25].However, the use of antioxidant vitamin and mineral sup-plements in AMD is controversial and further investiga-tion is necessary [25].

Identifying Neovascular AJvIDDirect ophthalmoscopy after pupillary dilation can

reveal features that suggest CNV secondary to AMD. Inparticular, the presence of drusen, especially if. they arenumerous (>20), soft, large (>63 11m),or confluent, car-ries a significant risk for the development of neovascularAMD [11]. Patients at risk of developing neovascularAMD should understand the nature of the disease and

self-test regularly, perhaps with an Amsler grid. TheAmsler grid (fig. 4), a printed grid of straight lines. is prob-

6 Gerontology ~OO3:-I<):I-II Ie

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ably a useful tool for monitoring the central visland can be used as a means to detect early, subtlchanges, as well as monitoring changes once thtbeen detected. The grid should be held at a norming distance and the patient should focus on thedot, one eye at a time (covering the other with theiwhile wearing any corrective vision aids that the)normally wear. Testing each eye separately hepatient to recognizevisual'symptoms that are in (

only. They should be asked to report any wavy, bndistorted lines, blurred vision, discolored lines, 0spots [26]. If distortions are detected with the Amslthe patient should be assumed to have CNV unle~is evidence to the contrary. These patients shouldpromptly by an ophthalmologist for treatment as tlhelp to minimize the risk of vision loss [27].

For patients with neovascular AMD in one epresence of five or more small drusen or one or mOldrusen in the fellow eye, focal hypel-pigmentation,tinfll or intraretinal blood or hemorrhage, or syhy~;ertension may increase the risk of CNV in theeye [11, 28]. Referral is advisable for these patitensure CNV is detected at aI).early stage.

Treatment Options for Neovascular AMD

During the 1990s, the Macu~ar PhotocoaglStudy (MPS) Group published' several papers srthat laser photocoagulation could be effective inpatients with neovascular AMD. Recently, photodytherapy with verteporfin (Visudyne@, Novartis AGknown as verteporfin therapy, has been approved jtreatment of selected cases of neovascular AMI

though there is no cure or preventative treatmeneovascular AMD at this time, these treatmen1reduce the risk of vision loss.

Laser PhotocoagulationAlthough laser photocoagulation may limit the I

of damage caused by neovascular AMD, it is applonly to a small subset of patients [29]. Strict eligibiliteria for treatment with laser photocoagulation reIthe composition. size, and location of the CNVAccordingly, this treatment has been recommendeuse in patients with juxtafoveal or extrafoveallesiowhom it confines lesion growth to a smaller areawithout treatment. The overall benefit of laser photgulation decreases as choroidal neovascular lesiortend towards the FAZ. When the CNV is subfoveal,photocoagulation can cause an immediate and perm,decrease in visual acuity due to destruction of the 0'

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~['ing healthy retinal photoreceptors, leaving an absolute1;scotOma [30]. Furthermore, a study showed that after 36.\ months, 82% of eyes with subfoveal CNV treated with~.laser photocoagulation were recorded as having a visual~ acuity of 20/200 or worse [30].Ie

~. Verteporfin Therapy

h Verteporfin therapy is a minimally invasive procedureI, that can be carried out on an outpatient basis by trained

(: ophthalmologists. It is a two-step process in which theiiidrug (verteporfin) is administered by intravenous infu-i( sion, then activated by a laser. After intravenous infusion,T verteporfin accumulates in the choroidal neovasculature.~.'A low-intensity, non-thermal laser that uses a specific~: wavelengthof light activates the drug, which can cause

highly localized damage to the choroidal neovasculature.~.The whole procedure takes approximately 20 minutes.g,Verteporfin has a short plasma half-life, which results int rapid clearancefrom the body [31].Becausethe laserused.IFto activate verteporfin is non-thermal, retinal function')!,may be maintained in areas overlying the verteporfin-tt treated choroidal neovascular lesions [32]. Verteporfin

therapy is therefore suitable for the treatment of substan-tially more patients with subfoveallesions than laser pho-tocoagulation, and without immediate loss of vision [13,

(x.33].IT Verteporfin therapy is approved for the treatment ofITneovascular AMD in patients with predominantly classicIi lesions (lesions in which the area of classic CNV is 2: 50%is of the area of the entire lesion on fluorescein angiography)h that are subfoveal [13, 34]. The 2-year results of the treat-~.'ment of AMD with photodynamic therapy (TAP) investi-'0 gation showed that verteporfin therapy significantly re-al duced the risk of moderate and severe vision loss in eyes

with predominantly classic sub foveal lesions at baseline[13]. In this subgroup, 65 (41%) of 159 verteporfin-treated eyes had lost at least 15 letters of visual acuity (the

n primary endpoint) compared with 57 (69%) of 83 eyes)\rf receiving placebo (p < 0.001) (fig. 5).ri' Recently, the verteporfin in photodynamic therapyfi (VIP) trial evaluated verteporfin therapy in patients with~t occult CNV secondary to AMD [35]. Data indicate thata verteporfin therapy is effective at reducing vision loss inil!patients with occult CNV with no classic CNV with pre-ar sumed recent disease progression.la Verteporfin therapy appears to be safe and well tolerat-:~ ed; most adverse events were mild to moderate and tran-

:e Slent in nature. Acute severe vision decrease (loss of 2:4ITlines of visual acuity within 7 days of treatment) occurredI)' III 1% of patients treated with verteporfin in the TAP

Common Eye Diseases of Elderly People

Treatment benefits of verteporfin therapy for neovascular AMD

- Vertepofin0 Placebo

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Fig. 5. A comparison ofthe percentage of eyes with at least moderatevision loss at the month 24 examination in patients with predomi-nantly classic lesibns at baseline in the TAP Investigation [13].

\investigation [13], and 4% of patients with AMD in theVIP trial [35]. Considering the large sample size of theTAP investigation, there were relatively few treatment-related ocular adverse events. Patitmts should be aware

that following verteporfin therapy, they may ~xperience aperiod of photosensitivity (3.5% of patients had photo-sensitivity reactions in TAP investigation) and shouldavoid exposure of unprotected skin or eyes to direct sun-light or bright indoor lighting (especially halogen lighting)for 48 hours.

One estimate suggests that verteporfin therapy willallow two J:o three times as many patients with CNV sec-ondary to AMD to be effectively treated than were pre-viously treatable [36]. This is likely to be an underesti-mate given the recent finding that verteporfin therapy hasbeen shown to be effective at reducing vision loss inpatients with occult CNV with no classic CNV with pre-sumed recent disease progression [35].

Cataract

Cataract, which is a lens opacity that interferes withvisual function, accounts for approximately 16 millioncases of blindness (visual acuity <20/400, Snellen equiva-lent) worldwide (World Health Organization 1997 esti-mate). The prevalence of vision loss caused by cataractincreases with age. In one study, the prevalence rose from

G~rontology 2003:49: I-II7

4.5% in people aged 52-64 years to 45.9()-IJin people aged75-85 years [37]. Also, the prevalence of cataract appearsto be highest in African Americans [38].

Signs and SymptomsA general blurring of vision (fig. 3) and sensitivity to

bright lights (table 1) are the characteristic symptomsreported for cataract [39]. Opacity of the lens can varyfrom a small local opacity to a diffuse general loss of trans-parency. Typically, the first changes a patient becomesaware of are clouding of the visual field, double vision, orboth [39]. As patients with cataract may experience pro-gressively worsening nearsightedness, frequent prescrip-tion changes for vision aids may be required. Unfortu-nately, as cataract progresses, stronger glasses can no lon-ger correct the worsening vision. Cataract can cause othervisual disturbances; for example, as color vibrancy dimin-ishes, the patient's vision may take on a yellow tint. Read-ing may become difficult because of reduce,d contrastbetween letters and their background [39]. Patients mayalso report that they cannot drive at night due to glarefrom the headlights of oncoming cars.

Although cataract is most commonly a result of aging,it may occur secondary to inflammation, trauma, diabetesmellitus, ultraviolet radiation, or metabolic or nutritionaldisorders [39-41]. Limited evidence suggests that vitaminsupplements, such as vitamins C, E, or B2 (riboflavin),may lower the risk of cataract - especially nuclear cataract[42, 43]. Benefits may be greatest if these nutrients areused for more than 10 years; however, the specific nu-trients that may be responsible for lowering the risk ofcataract have not been identified [43].

Treatment OptionsEarly detection is important because cataract is a pro-

gressive disease that is associated with a correspondingprogressive decrease in vision. Vision aids can decreaseglare, increase image contrast, correct for refractive er-rors, and correct for differences in vision between theaffected and unaffected eye in patients with cataract. Theextent of visual disability will determine the need for sur-gical intervention to remove cataract. Cataract surgery isassociated with a small risk of vision decrease or perma-nent vision loss; however, standard cataract extractionwith intraocular lens implantation results in improvedvision in most patients [44].

8 Gerontology 2003:49: 1-11 t!I

Glaucoma

Approximately 6.4 million people worldwidefected by blindness due to glaucoma (World Healnization 1997 estimate). Of those people who arblind (visual acuity of 20/200 or worse in the betteeye) because of glaucoma, 75% are older than 65age [45]. - --

Glaucoma can be classified into two broad typeangle and angle-closure, each of which can be categcprimary or secondary. When the cause of glaucorrknown, it is termed primary glaucoma; it isclassifieondarywhen the condition is due to another cause. Iopen-angle glaucoma presents with characteristic I

ofthe optic nerve, whereas inprimary angle-closurema, the peripheral part of the iris bunches up agatrabecular meshwork (spongy tissue located nearnea) and prevents aqueous from draining from the;chamber causing high intraocular pressure [46]angle glaucoma accounts for 80% of all glaucoma c,

be2pmes more common as age increases [47].

Signs and SymptomsElevated intraocular pressure, reduced visu

(fig. 3), and optic nerve cupping indicate that amay have glaucoma (table 1). The rate of progre~glaucoma d~pends on the level of inJraocular presssusceptibility of the optic nerve to damage, and thety of the disease. The mild and moderate stagetypes of glaucoma are normally asymptomatic. H<as the disease progresses, visual field defects devthe area of peripheral vision and spread to createvision - central vision may be affected late in theprocess [46]. The patient may report that they anthat parts of objects appear to be missing (e.g. tletters of words). They may also complain ofvision or eye pain, particularly after vigorous e:Headaches while reading or during low levels of illtion are suggestive of glaucoma, especially if accomwith misty vision or haloes. Poor color percepti,reduced night vision may also suggest glaucoma.

The risk of glaucoma is greater in certain grcpeople. Age is the greatest risk factor for the develcof glaucoma; prevalence is four to ten times higherpIe over 40 years of age [48]. Also, patients witintraocular pressure (> 21 mm Hg) are much monto develop glaucoma [48]. Other factors that are ased with glaucoma include: race, family history, higlpressure, diabetes mellitus, high myopia, and ocupertension [49].

Harvey

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Treatment OptionsCurrent treatment for open-angle glaucoma usually

at\beginswith pharmacological intervention, leading to laserr~trabeculoplasty or surgery, when necessary. The purposea~ofeach treatment is to lower the intraocular pressure. The:i1'}~rnost.commonlyused classes of drugs for open-angle glau-r_coma are beta-adrenergic antagonists, alpha2-adrenergic~agonists, parasympathomimetic agents, carbonic anhy-

le~drase inhibitors, and prostaglandin-receptor agonists., ,j~~

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,However, these medications may cause systemic side,<

u~effects. For angle-closure glaucoma, the treatment se-

;fquence is as follows: pharmacological intervention, pe-a~ripheral iridotomy, and, if necessary, filtration surgeryi~;[49].For both open-angle and angle-closure glaucoma, the

c1~sequenceof treatment opt,ions is designed to maximizetllthe benefit of the treatment, while minimizing the risk ofo~harm to the patient. However, as glaucoma is a chronic,

'ilprogressive disease with no known cure, many patientse~;l11ayrequire all three treatment options. Patients must be

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Diabetic Retinopathy

I Diabetic retinopathy is the most serious sight-threaten-th~,jngcomplication of diabetes mellitus and accounts for

~~about 2.4 million cases of blindness globally (WorldM!HealthOrganization 1997 estimate). It can be classified,'e(~basedon the extent of proliferation of new blood vessels,ufintotwo broad categories - nonproliferative diabetic reti-

n.lmopathy and proliferative diabetic retinopathy. In pa-,~tients with non proliferative diabetic retinopathy, progres-,~sion to the more severe proliferative form may occur.rliMicroaneurysms, intraretinal hemorrhages, soft exudates,.~;hard exudates, intraretinal microvascular abnormalities,sl~venouslooping, or venous beading characterize the non-la~proliferativeform [50]. The most common cause of visionetloss in non proliferative diabetic retinopathy is macularnftedema [51]. Proliferative retinopathy is characterized byI~roliferating endothelial cell tubules, fibrous prolifera-(}1tlOn,intra- or peri-retinal hemorrhage, or vitreous hem or-:~rhage. There is significant risk of vision loss in patients~~'withproliferative retinopathy [50]. One study found that~the prevalence of blindness (visual acuity of 20/200 or~lfworse)and visual impairment (visual acuity of 20/40 oral#worse)due to diabetic retinopathy was higher in older~patients than younger patients [51]. The 10-year inci-l~dence of blindness for people whose diabetes was classed

as younger-onset «30 years of age when diagnosed),

~ Common Eye Diseases of Elderly People

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older-onset (2: 30 years of age when diagnosed) insulin-dependent, and older-onset non-insulin-dependent was1.8%,4.0%, and 4.8%, respectively; 10-year incidences ofvisual impairment were 9.4%, 37.2%, and 23.9%, respec-tively.

Signs and Symptoms ,

Some patients will notice a change in central (fig. 3) orcolor vision. Blurred or distorted vision, and reduced cen-tral vision may be reported by patients with macular ede-ma (fig. 2) [51]. Patients may notice very small graypatches or spots in the visual field and their visual acuitymay be worse in the morning than in the afternoon. How-ever, for most patients with diabetic retinopathy, thereare no early symptoms. Many patients do not develop anyvisual impairment until the disease has advanced wellinto the proliferative stage. At this stage of the disease,vision that has l;>eenlost cannot be restored.

Early detection of diabetic retinopathy is essential as~arly treatment can reduce the risk of severe vision loss.Patients at high\risk of diabetic retinopathy should beencouraged to uriVergo annual screening for the disease.All patients with diabetes mellitus should have annualfundus examinations (after dilation of the pupil), andyearly examinations are recommended for patients withdiabetic retinopathy [50]. Nearly all patients with dia-betes mellitus will develop diabetic retinopathy" so it isimportant for them to learn about the disease process andthe risks of developing ocular signs and symptoms thatmay accompany vision loss.

Treatment OptionsDietary and pharmacological interventions aimed at

controlling blood sugar levels should be combined as themainstay 61'treatment to prevent retinopathy [52]. Forpatients with insulin-dependent diabetes, intensive man-agement to normalize blood sugar levels can delay theonset and slow the progression of clinically important reti-nopathy, including vision-threatening lesions, by more,than 70% [53].

Macular edema is a frequent complication in patientswho have diabetes and may be associated with loss ofvision. Focal laser photocoagulation of clinically signifi-cant macular edema may reduce the risk of vision loss inthese patients [50]. Furthermore, controlling blood pres-sure and cholesterol levels may reduce the risk of clinical-ly significant edema [51].

Scatter laser photocoagulation surgery can reduce therisk of severe vision loss by 50-60(}h in patients with pro-liferative retinopathy and can also be considered in pa-

Gerontology 2003;49: I-II.

9

tients with older-onset diabetes with severe nonprolifera-tive retinopathy that appears to be approaching prolifera-tive retinopathy [54]. The laser beam is used to makehundreds of small burns over the retinal surface that

destroy the new, growing blood vessels. Cloudy vision canbe treated by vitrectomy, a surgical procedure that clearshemorrhaged blood.

References

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;:1

'i: 1

I Thylefors B, Negrel AD, Pararajasegaram R,Dadzie KY: Global data on blindness. Bull

World Health Organ 1995;73:115-121.2 Manton KG, Stallard E: Cross-sectional esti-

mates of active life expectancy for the U.S.elderly and oldest-old populations. 1 Gerontol1991;46:SI70-S182.

3 Rovner BW, Zisselman PM, Shmuely-DulitzkiY: Depression and disability in older peoplewith impaired vision: a follow-up study. 1 AmGeriatrSoc 1996:44:181-184.

4 Brown GC, Brown MM, Sharma S: Differencebetween ophthalmologists' and patients' per-ceptions of quality of life associated with age-related macular degeneration. Can 1 Ophthal-mol 2000;35: 127-133.

5 Bressler NM, Bressler SB, Fine SL: Age-relatedmacular degeneration. Surv Ophthalmol 1988;32:375-413.

6 Hyman L: Epidemiology of AMD; in HamptonGR. Nelsen PT (eds): Age-related Macular De-generation: Principles and Practice. New York,Raven Press, 1992,pp 1-35.

7 Bressler NM, Bressler SB, Gragoudas ES: Clini-cal characteristics of choroidal neovascular

membranes. Arch Ophthalmol 1987;105:209-213.

8 Stevens TS, Bressler NM. Maguire MG, Bressl-cr SB, Fine SL Alexailder 1, Phillips DA,Margherio RR, Murphy PL Schachat AP: Oc-cult choroidal neovascularization in age-relat-ed macular degeneration. A natural historystudy. Arch Ophthalmol1997: 115:345-350.

9 Sunness lS, Gonzalez-Baron 1, Applegate CA,Bresslcr NM, Tian Y, Hawkins B, Barron Y,Bergman A: Enlargement of atrophy and visualacuity loss in the geographic atrophy form ofage-related macular degeneration. Ophthal-mology 1999;106:1768-1779.

10 Bressler SB, Bressler NM. Fine SL. Hillis A,Murphy RP. Olk Rl, Patz A: Natural course ofchoroidal neovascular membranes within the

foveal avascular zone in senile macular degen-eration. Am 1 OphthalmoI1982:93: 157-163.

II,L

Ii1'1

Conclusions

AMD, cataract, glaucoma, and diabetic reiare common causes of reduced vision in peopleover the age of 50 years. Early detection and treathese conditions are important because they canoutcome. By being alert to the early signs and syof these eye diseases, geriatriciap.s have an importo play in their management. Geriatricians are,position to raise awareness of the symptoms oftbcauses of blindness among elderly patients so tlmay report symptoms more readily instead of mthat vision loss is an inevitable, and untreatable, aaglllg.

II Pieramici Dl, Bressler SB: Age-related maculardegeneration and risk factors for the develop-ment of choroidal neovascularization in the fel-

low eye. Curr Opin Ophtl\almoI1998;9:38-46.12 Brown GC, Murphy RP:'Yisual symptoms as-

sociated with choroidal "neovascularization.

Photopsias and the Charles Bo)1net syndrome.Arch OphthalmoI1992;110:1251:"1256.

13 Treatment of Age-Related Macular Degenera-tion with Photodynamic Therapy (TAP) StudyGroup: Photodynamic therapy of subfovealchoroidal neovascularization in age-relatedmacular degeneration with verteporfin: two-year results 01'2 randomized clinical trials-TAPReport 2. Arch Ophthalmol 2001;119:198-207.

14 Alexander MF, Maguire MG, Lietman TM,Snyder lR, Elman Ml, Fine SL: Assessment ofvisual function in patients with age-related ma-cular degeneration and low visual acuity. ArchOphthalmoI1988;106:1543-1547.

15 Ivers RQ, Cumming RG, Mitchell P, Attebo K:Visual impairment and falls in older adults: theBlue Mountains Eye Study. 1 Am Geriatr Soc1998;46:58-64.

16 Klein BE. Klein R, Lee KE. Cruickshanks KJ:Performance-based and self-assessed measures

of visual function as related to history of falls.hip fractures, and measured gait time. TheBeaver Dam Eye Study. Ophthalmology 1998;105: 160-164.

17 AMD Alliance International. Awareness re-

search. 1999. http://www.amdalliance.orgiam d/awareness_research.html.

18 Butler RN, Faye EE. GuazzoE, Kupfer C:Keeping an eye on vision: new tools to preservesight and quality of life. A roundtable discus-sion. Part 2. Geriatrics 1997;52:48-56.

19 Smeeth L: Assessing the likely etTectiveness ofscreening older people for impaircd vision inprimary carc. Fam Pract 1998; 15:S24-S29.

20 Klein R. Klein BE. Linton KL: Prevalence of

age-related maculopathy. The Beaver Dam EyeStudy. Ophthalmology 1992:99:933-943.

10 Gerontology 2003:49: I-II~

21 Klein R, Rowland ML, Harris MI: Rnic differences in age-related macThird National Health and Nutritio

nation Survey. Ophthalmology 1995;381.

22 Zhang K. Nguyen TH, Crandall A, DcGenetic and molecular studies of mac

trophies: recent developments. SUfvmol 1995;40:51-61.

23 Moeller SM, lacques PF, Blumbergpotential role of dietary xanthophyll,ract and age-related macular degeneAm Coli Nutr 2000; 19:522S-527S.

24 Newsome DA:Swartz M, Leone NCRC, Miller E: Oral zinc in macular dtion. Arch Ophthalmol1988; 106: 192~

25 Evans lR: Antioxidant vitamin and

supplements for age-related macula!eration. Cochrane Database Syst ReCDOO0254.

26 Fine AM. Elman Ml. Ebert lE, Pre:Starr lS, Fine SL: Earliest symptoms c,neovascular membranes in the macu

OphthalmoI1986;104:513-514.27 Alexander LJ: Age-related macular d.

tion: the current understanding of the ~clinicopathology. diagnosis and managlAm Optom Assoc 1993;64:822-837.

28 Macular Photocoagulation Study GrOlfactors for choroidal neovascularizatio

second eye of patients with juxtafovealfoveal choroidal neovascularization sel

to age-related macular degeneratiorOphthalmoI1997;115:741-747.

29 Ciulla TA, Danis RP. Harris A: Agemacular degeneration: a review of exp'tal treatments. Surv Ophthalmol 1998;'146.

30 Macular Photocoagulation Study Groulphotocoagulation of subfovealneovascsions of age-related macular degeneratidated findings from two clinical trialOphthaII11011993;111:l200-1209.

Harvey

Houle J. Bain S. Azab M. Strong A: Clinical

phannacokinetics of verteporfin in healthy vol-unteers and patients with CNV. Invest Oph-thalmol Vis Sci 2001;42:S437.Schmidt-Erfurth U, Miller J, Sickenberg M,Bunse A, Laqua H, Gragoudas E, Zografos L,Birngruber R. van den BH, Strong A. ManjurisU. Fsadni M, Lane AM, Piguet B, Bressler NM:photOdynamic therapy of sub foveal choroidalneovascularization: clinical and angiographicexamples. Graefes Arch Clin Exp Ophthalmol1998:236:365-374.Macular Photocoagulation Study Group: Ar-

gon laser photOcoagulation for neovascular ma-culopathy: three-year results from randomizedclinical trials. Arch Ophtha]mol 1986;I04:694-701.Treatment of Age-Related Macular Degenera-tion with Photodynamic Therapy (TAP) Study

Group: Photodynamic therapy of subfovealchoroidal neovascularization in age-relatedmacular degeneration with verteporfin: one-

year results of2 randomized clinical trials-TAPReport 1. Arch Ophthalmol 1999;117:1329-1345.Verteporfin In Photodynamic Therapy StudyGroup: Verteportin therapy of sub fovea! cho-roidal neovascularization in age- related macu-lar degeneration: two-year results of a random-ized clinical trial including lesions with occultwith no classic choroidal neovascularization-

Verteporfin In Photodynamic Therapy Report2. Am J OphthalmoI2001;J31:541-560.Margherio RR, Margherio AR, DeSantis ME:Laser treatments with vertepomn therapy andits potential impact on retinal practices. Retina2000;20:325-330.

)mmon Eye Diseases of Elderly People

37 Kahn HA. Leibowitz HM, Ganley JP, KiniMM. Colton T. Nickerson RS. Dawber TR:

The Framingham Eye Study. I. Outline andmajor prevalence findings. Am J Epidemiol1977;106:17-32.

38 Klein BE, Klein R: Cataracts and macular de-generation in older Americans. Arch.Ophthal-mol 1982;100:571-573.

39 The American Optometric Association Con-sensus Panel on Care of Adult Patients with

Cataract. Optometric clinical practice guide- ,line care of the adult patient with cataract.1995. www.aoanet.orglcpg-9-cpoag.htmL

40 Cohen DL. Neil HA, Sparrow J. Thorogood M,Mann JI: Lens opacity and mortality in dia-betes. Diabet Med 1990;7:615-617.

41 Jacques PF. Chylack LT, Jr., McGandy RB,Hartz SC: Antioxidant status in persons withand without senile cataract. Arch Ophthalmol1988: 106:337-340.

42 Cumming RG, Mitchell P, Smith W: Diet andcataract: the Blue Mountains Eye Study. Oph-thalmology 2000;107:450-456.

43 Mares-Perlman JA. Lyle BJ, Klein R, FisherAI, Brady WE, VandenLangenberg GM, Tra-bulsi IN, Palta M: Vitamin supplement use andincident cataracts in a population-based study.Arch Ophthalmol 2000;118:1556-1563.

44 Revicki DA. Brown RE. Adler MA: Patient

outcomes with co-managed post-operative careafter cataract surgery. J Clin Epidemiol 1993;46:5-15.

45 Pizzarello LD: The dimensions of the problemof eye disease among the elderly. Ophthalmolo-gy 1987;94:1191-1195.

46 Quillen DA: Common causes of vision loss inelderly patients. Am Fam Physician 1999;60:99-108,

47 Abyad A: In-office screening for age-relatedhearing and vision loss. Geriatrics 1997;52:45-57.

48 Leibowitz HM, Krueger DE, Maunder LR,Milton RC, Kini MM, Kahn HA, NickersonRJ, Pool J, Colton TL. Ganley JP, LoewensteinJI, Dawber TR: The Framingham Eye Studymonograph: An ophthalmological and epide-mio]ogical study of cataract. glaucoma. diabet-ic retinopathy, macular degeneration, and vi-sual acuity in a general population of 263]adults, 1973-1975. Surv Ophthalh101 1980:24:335-610. .

49 The American Optometric Association Con-

sensus Panel on Care of the Patient with OpenAngle Glaucoma: Optometric clinical practiceguideline care of the patient with open angleglaucoma. 1995.

50 The American Optometric Association Con-sensus Panel on Diabetes: Optometric clinicalpractice guideline care of the patient with dia-betes mellitus. 1993.

51 Moss Sf, Klein R, Klein BE: Ten-year inci-dence of visual loss in a diabetic population.Ophthalmology 1994;101:]061-1070.

52 Cooppan R: Diabetes in the elderly: implica-tions of the diabetes control and complicationstriaL Compr Ther 1996;22:286-290.

~3 The Diabetes Control and Complications Trial

\ Research Group: The effect of intensive treat-ment of diabetes on the development and pro-gression of long-term complications in insulin-dependent diabetes mellitus, N Engl J Med1993;329:977-986. '

54 Early Treatment Diabetic Retinopathy StudyResearch Group: Early photocoagulation fordiabetic retinopathy. ETDRS report number 9.

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Gerontology 2003:49: I-II""

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