Comprehensive Guide to Cataracts and Their Treatment Options

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

3. 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.

4. Cataracts • Definition and Symptoms of Cataracts. • Clouding of the lens which prevents light from passing through properly to the retina • Types -3

5. 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

6. 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)

7. 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

8. Cataracts • Peri-operative complications • Hypertension • Arrhythmia • 31 complications per 1000 procedures

9. 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

10. 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

11. 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

12. 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.

13. 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

14. Cataracts • Future – • Laser, ultrasound – less heat generated, • Pulse phacoemulsification – less heat – less chance for wound burn

15. 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%)

16. 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

17. 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

18. 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

19. 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

20. 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

21. 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

22. 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.

23. 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

24. 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)

25. 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.

26. Glaucoma • Cannabinoids • 1971- smoking marijuana lowers intraocular pressure by 45% • No successful topical form and systemic causes too many side effects

27. 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

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

29. Macular Degeneration • 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

30. Macular Degeneration • 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

31. Macular Degeneration • 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

32. Macular Degeneration • Geographic pattern of retinal pigment epithelial atrophy

33. Macular Degeneration • Disruption of Bruch’s membrane- • Choroidal neovascularization- edema – disruption of visual function – wet type or exudative age related MD

34. Macular Degeneration • 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

35. Macular Degeneration • Retinal and choroidal angiography • Intraretinal hemorrhage and edema of macula • Fluorescein angiogram with leakage • Indocyanine green angiogram – choroidal vasculature

36. Macular Degeneration • 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

37. Macular Degeneration • 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

38. 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