The Aging Eye January 5, 2004 Dorothy D. Sherwood, M.D.

The Aging Eye

January 5, 2004

Dorothy D. Sherwood, M.D.

Cataracts

• Cataracts are the leading cause of blindness world wide.

• Cataract surgery is the most frequently performed surgical procedure in the US with 1.5 million operations annually

• 50% of those over 65 develop vision impairing cataracts.

Cataracts

• Definition and Symptoms of Cataracts. – Clouding of the lens

which prevents light from passing through properly to the retina

– Types -3

Cataracts

• Nuclear Cataracts– Most common age-related cataract

• Substantial genetic component• Age, female sex, smoking are risk factors• More common in white

• Cortical– Related to sun exposure– More common in blacks

• Posterior Subcapsular– steroids

Cataracts

• Symptoms:– Cloudy vision, glare, halos, decreased night

vision, faded colors, double vision, need for brighter light when reading

• Treatment – can neither be prevented or treated with medications – surgical only– Removal of lens and insertion of intraocular

lens (permanent)

Cataracts

• Indications for surgery– When visual impairment interferes with ADL’s, driving,

working, – Co-existing ocular conditions requiring removal for

treatment such as macular degeneration, diabetic retinopathy, glaucoma

• Peri-operative evaluation- none– 19000 cases – no improved outcome with pre-

operative evaluation, except MI within 3 months– No need to stop anticoagulants or ASA-Archives –

April 28, 2003 – 163(8):901-908

Cataracts

• Peri-operative complications– Hypertension– Arrhythmia– 31 complications per 1000 procedures

Cataracts

• Surgical Strategies– Dilate eye and wash with povidone-iodine

solution – Small self-sealing corneal or scleral incision is

made for phacoemulsification tip and IOL – Injection of viscous material into anterior

chamber to maintain the stability of the eye– Open the capsule with continuous tear

capsulotomy, inject saline, separate lens from capsule with phacoemulsification

Cataracts

• Phacoemulsification introduced by Kelman in 1967– Ultrasound probe using piezoelectric crystals

to convert electrical energy into mechanical energy

• Irrigation and aspiration of the cataract. The posterior capsule is kept intact.

• Anesthesia is usually 1% lidocaine topical

Cataracts

• IOL– First implanted by Ridley in 1949– Currently it is a small, foldable silicone or

acrylic material injected into the capsule.– Monofocal or multifocal lens are available

• Monofocal – distant vision only, near vision requires glasses

• Multifocal – both – however, halos and loss of clarity are down side

Cataracts

• Postoperative Care– Topical eye drops

• Antibiotics – gatifloxacin or moxifloxacin• Steroids for inflammation –prenisolone acetate 1%• NSAI drops – ketorolac tromethamine0.5% to

prevent inflammation in the retinal • Examined one day, one week, two weeks, 1

months and 3 months post op – glasses can be prescribed in 2 weeks.

Cataracts

• Risk Benefits:– Bleeding, infection, posterior dislocation of lens

material- intraoperative– Post operative -High-level of pressure in the eye,

corneal swelling, retinal inflammation, dislocation of the IOL, retinal detachment, infection

– Posterior capsule opacifications (PCO) – migration of lens remnants to the visual axis of the capsule – less common with improved technique – treat with laser

Cataracts

• Future –– Laser, ultrasound – less heat generated, – Pulse phacoemulsification – less heat – less

chance for wound burn

Cataracts

• Take home– Most common cause of blindness worldwide, affecting

50% of the over 65 population– Clouding of the lens which impairs light travel to the

retina. – Age, female sex, smoking, white – nuclear– Black, sun exposure – cortical– Steroids – subcapsular– MI 3 months prior is only risk factor- no preop

evaluation needed. – Post op meds: gatifloxacin or moxifloxacin,

prenisolone acetate 1%, and ketorolac tromethamine0.5%)

Glaucoma

• The triad of increased intraocular pressure, degeneration of the optic nerve head, restricted visual field – open angle glaucoma

• Visual impairment in 0.7% of those over 60, 4% of those over 90

• IOP greater than 17.5 mmHg is associated with a persistent loss of vision and underscores the need to aggressively treat intraocular pressure

Glaucoma

• Diagnosed before loss of vision by ophthalmoscopic examination of the optic nerve to detect cupping. – Blacks– Advanced age– Family history– Elevated intraocular pressure- Goldman’s tonometer

is gold standard – but the Schiotz indentation tonometer is cheap and easy to use – normal pressure is 15 to 16 mmHg – those with pressures over 21 are considered to have ocular hypertension

Glaucoma

• Dynamics of aqueous humor:– Produced by ciliary

body, circulates around lens, through pupil, and anterior chamber

– Flows out through the trabecular meshwork into the venous system –here-in lies the problem

Glaucoma

• Treatment is started when there is optic disc cupping or even when there is just elevated pressure >21 (normal 15).

• The remainder of this discussion on glaucoma will cover the drugs used to treat this problem

Glaucoma

• Pharmacopoeia

– Topical inhibition of carbonic anhydrase– Agonism of the alpha-adrenoceptor – Safer beta-adrenoceptor antagonist– Prostaglandin Analogues– Enhancement of trabeuclar outflow and

uveoscleral outflow

Glaucoma

• Carbonic Anhydrase Inhibitors-sulfonamides- 1 drop tid– Inhibition of carbonic anhydrase in the eye results in

decreased fluid transport across the ciliary body resulting in decreased formation of aqueous humor

– Dorsolamide (Trusopt), brinzolamide (Azopt)- as effective as timolol, additive to timolol, brinzolamide is less irritant as its pH is 7.5 vs 5.6

– Burning, stinging, bitter taste, 15% - allergic conjunctivitis

Glaucoma

• [beta]-Adrenoceptor Antagonist-– Timolol – (Timoptic) – used since 1979-

lowers intraocular pressure – the method of action is unknown, but may be related to decrease in aqueous humor production

– Contraindicated in asthma, severe COPD, bradycardia, third degree heart block, CHF

– Betaxolol – (Betoptic or Kerlone)- may have decreased bronchoconstriction and causes increased retinal blood flow.

Glaucoma

• Combination therapy– Dorsolamide and timolol (Corsopt) – decreases

pressure by 50%

• [alpha]-Adrenoceptor Agonists– Stimulate presynaptic feedback inhibition of

norepinephrine and reduce aqueous humor formation.– .125% clonidine tid equal to pilocarpine, the standard

• Doses of .25% or .5% produced hypotension– Brimonidine-(Alphagan)- reduces AH production, but

also increases uveoscleral outflow - .2% tid – as effective as timolol

• Headache, dry mouth, fatigue, ocular discomfort

Glaucoma

• Prostaglandin Analogs;– Latanoprost (Xalatan) –approved in 1996 –

more effective than timolol bid and is only dosed qd. Causes increased pigmentation, growth of eyelashes, conjuctival hyperemia

– Enhance uveoscleral outflow– Other drugs in same class:

• Unoprotatone(Rescula), travoprost (Travatan), bimatoprost (Lumigan)

Glaucoma

• Muscarinic agents – parasympathomimetic drugs have been used since 1870’s. – Contraction of the muscle of the ciliary body – pulls

scleral spur, opens trabecular meshwork, and increases aqueous flow form the eye

– These agents are anticholinesterases • Pilocarpine -.25% to 4% every 4 to 8 hours as needed• Cause miosis and cataracts• Ocusert- wafer placed under the lid once a week – less side

effects.

Glaucoma

• Cannabinoids– 1971- smoking marijuana lowers intraocular

pressure by 45%– No successful topical form and systemic

causes too many side effects

Glaucoma

• Take home points– DX and TX early – Schiotz tonometer, cupping of

disc. – Risk: Age, black, family history– Drugs: CAI – decrease AH – Dorsolamide– Alpha agonist – decrease AH - Brimonidine– Beta blocker – unknown- Timolol– Prostaglandin analog- scleral-uveal –Lantaoprost– Muscarininc- opens the trabecula - Pilocarpine

Macular Degeneration

• Most common cause of blindness in the Western World – 8 million people world wide.


• Macula is 5.5 mm in diameter, fovea is at its center – located temporally from the optic disc.

• Fovea is thinnest part of the retina – no blood vessels

• Preponderance of cone cells – detailed central vision


• The retina is functionally 2 layers– Rods and cones – connected to the optic

nerve– Retinal pigment epithemlium and its basal

lamina called Bruch’s membrane – maintains the integrity of the barrier between the choroid and the retina

– The choroid is between the retinal and the sclera


• Causes:– Risk factors : age, soft drusen, macular pigmentary

change, chorioidal neovascularisation in the other eye, hypertension, smoking, family history

– The retinal pigment epithelium becomes less efficient – results in accumulation of waste material called drusen. The retinal pigment cells degenerate and central vision is lost

– This is dry type age related MD – slowly progressive – 5 to 10 years to blindness


• Geographic pattern of retinal pigment epithelial atrophy


• Disruption of Bruch’s membrane-– Choroidal

neovascularization- edema – disruption of visual function – wet type or exudative age related MD


• Clinical features– Blurring of the central vision– Reduced vision, metamorphopsia

• The lines on graph paper will appear wavy or distorted

– Ophthalmoscopic examination – chorioretinal atrophy on dry or macular edema on wet type, associated with retinal hemorrhages and lipid exudate


• Retinal and choroidal angiography– Intraretinal

hemorrhage and edema of macula

– Fluorescein angiogram with leakage

– Indocyanine green angiogram – choroidal vasculature


• Clinical Advances– Laser treatments for choroidal neovascularization– Radiation treatment may preserve near vision and

contrast sensitivity– Prevention: High dose Zn and Vit A,C,E– Lutein and zeaxanthin carotenoids – potent native-

antioxidants found in high concentration in the macula – needs to be studied

– Suppression of vascular endothelial growth factor or other antiangiogenic agents


• Take Home Points– Risk – age, soft drusen, htn, smoking, family

history– Retina – retinal pigmented epithelium and

rods and cones– Dry – failure of the RPE to remove waste

products – results in accumulation of stuff-atrophy

– Wet- neovascularization of the Choroid –breaks Burch’s membrane-edema

The Aging Eye

• References:– “Age related macular degeneration”; BMJ Volume

326(7387); March 1 2003; pp 485-488– “Recent Advances and Future Frontiers in Treating

Age-Related Cataracts”; JAMA volume 290(2); July 9, 2003; pp248-251

– “Drug Therapy-Medical Management of Glaucoma”; volume 339(18); October 29 1998; pp1298-1307

– “New Glaucoma Medications in the Geriatric Population: Efficacy and Safety”; JAGS volume 50(5) May 2002; pp 956-962

The Aging Eye January 5, 2004 Dorothy D. Sherwood, M.D.

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