1 / 38

The Aging Eye

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

laurawatson
Download Presentation

The Aging Eye

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


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

  2. 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.

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

  4. 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

  5. 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)

  6. 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

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

  8. 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

  9. 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

  10. 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

  11. 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.

  12. 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

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

  14. 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%)

  15. 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

  16. 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

  17. 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

  18. 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

  19. 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

  20. 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

  21. 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.

  22. 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

  23. 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)

  24. 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.

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

  26. 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

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

  28. 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

  29. 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

  30. 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

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

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

  33. 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

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

  35. 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

  36. 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

  37. 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

More Related