The Aging Eye

=Objectives=

Gradual Onset Painless Vision Loss

 * Cataract
 * Primary Open Angle Glaucoma
 * Age-related Macular Degeneration
 * Diabetic Retinopathy

Cataract

 * Clouding of the lens, blurry vision, decreased contrast sensitivity
 * Patients have difficulty reading (need more light), seeing at night, and have problems with the glare from oncoming headlights
 * There is a myopic shift (also called prodromal myopia). This means that the ability to do close work without glasses returns, and is a common symptom of developing cataracts.
 * Surgery
 * Topical anesthetic given
 * Phacoemulsification uses ultrasound power
 * 2-3 mm corneal incision
 * Takes 20-30 minutes
 * Post-op activity restrictions are minimal
 * Basically, the old cataract is removed and is replaced with an intraocular lens. It is usually successful with >90% enjoying improved vision.

Open Angle Glaucoma

 * Glaucoma
 * A form of optic nerve damage with loss of optic nerve tissue
 * Often, but not always, associated with increased eye pressure
 * Can lead to peripheral vision loss and eventually central vision loss
 * Mainly a disease of the elderly
 * Family history is important
 * Two types: open angle glaucoma and angle closure glaucoma, we care about open angle today
 * Open Angle Glaucoma
 * Commonly has no symptoms
 * When symptomatic, presenting symptom is peripheral vision loss
 * Central vision unaffected until late
 * There is rarely pain
 * There is a slow onset
 * Check by screening for glaucoma by checking intraocular pressure and optic nerve appearance
 * Progressive thinning of the rim of the nerve, loss of nerve tissue and increased cup to disc ratio are indicative of the disease
 * The anatomy of the nerve fiber layers in the optic nerve leads to the peripheral to central pattern of vision loss seen in glaucoma
 * Medications
 * Beta blockers: decrease aqueous production. Timolol
 * Carbonic anhydrase inhibitors: decrease aqueous production. Dorzolamide
 * Prostaglandin analogues: increase vascular outflow of aqueous. Latanoprost
 * Alpha adrenergic agonists: increase outflow of aqueous, decrease aqueous production. Brimonidine
 * Surgical options as well (shunts and trabeculectomy)

Age-Related Macular Degeneration

 * 85-90% is in the "dry" form
 * Drusen are yellow deposits of lipofuscin in the macula are characteristic
 * Atrophy to the central retinal pigment epithelial layer below the retina, causing vision loss through loss of photoreceptors, loss of central vision
 * Vision loss is slowly progressive
 * 10-15% is the "wet" form
 * Bleeding and leaking of blood vessels under the retina
 * Due to abnormal blood vessel growth
 * Causes rapid vision loss if untreated
 * The worse of the two options
 * New treatments: ranibuizumab and pegaptanib are FDA approved. Bevacizumab is not FDA approved, but used off-label.  All are used commonly know, apparently to great effect.  Side note, bevacizumab is only $150 per treatment, while ranibuizumab is about $2k per treatment.  wow.
 * There is some evidence that taking nutritional supplements (Vit C, E, beta-carotene, zinc oxide and copper) helped decrease developing AMD. This Cochrane Review article   "Antioxidant vitamin and mineral supplements for slowing the progression of age-related macular degeneration" .questions that conclusion.

Non-Proliferative Diabetic Retinopathy

 * Fluid leaks through the blood vessels into the retina causing macular swelling and decreased central vision
 * Treated using laser photocoagulation or intravitreal injections

Acute Onset Painless Vision Loss

 * Acute onset painless vision loss in diabetics
 * Central retinal artery occlusion
 * Branch Retinal Artery Occlusion
 * Central of Branch Retinal Vein Occlusion
 * Anterior Ischemic Optic Neuropathy

Acute onset painless vision loss in diabetics

 * In severe hyperglycemia, can have refractive shift causing poor vision
 * Usually goes away over time
 * Often seen around the time of diagnosis of diabetes if there is prolonged elevated blood sugar

Central retinal artery occlusion

 * Retinal arterial embolus
 * Risk factors are atherosclerosis and HTN
 * Clinical signs are: poor vision (usually vision loss), afferent pupillary defect, cherry red spot, and narrowed retinal arterioles
 * Poor prognosis

Branch Retinal Artery Occlusion

 * Vision is variable
 * The afferent pupillary defect is mild or absent

Central of Branch Retinal Vein Occlusion

 * Vascular turbulence of at the optic nerve head causes endothelial damage and thrombus formation
 * Seen with increasing age, HTN, DM, abnormalities of coagulation, glaucoma
 * Very poor vision, afferent pupillary defect, venous turtuosity and engorgement, extensive retinal hemorrhages

Anterior Ischemic Optic Neuropathy

 * Loss of vision due to damage to the optic nerve from insufficient blood supply.
 * Can result in: vision loss, visual field defect, optic disc edema
 * Types: arteritic (caused by Temporal Arteritis) and non-arteritic (not caused by Temporal Arteritis)
 * Arteritic Anterior Ischemic Optic Neuropathy
 * Caused by Temporal Arteritis
 * Important cause of vision loss in elderly
 * Inflammation or thrombotic occlusion of short posterior ciliary arteries supplying optic nerve
 * Symptoms are: temporal headaches, scalp tenderness, jaw claudication, malaise, anorexia, weight loss, fever, joint and muscle pain
 * Transient dimming of vision or vision loss may occur
 * Specific etiology of vision loss can be: arteritic anterior ischemic optic neuropathy, posterior ischemic optic neuropathy, or central retinal artery occlusion
 * Work up with ESR, CRP, CBC, Temporal artery biopsy
 * Treat by starting steroids
 * Polymyalgia Rheumatica is sometimes associated with it (Thanks Parimal's dad for that gem, and wikipedia for backing him up)
 * Non-Arteritic Anterior Ischemic Optic Neuropathy
 * Not in the setting of temporal arteritis
 * Often have altitidunal visual field defect
 * Segmental disc edema
 * Risk factors include: small cup-to-disc ratio, HTN, DM, hyperlipidemia, CRF, smoking
 * Start ASA

Transient Vision Loss

 * Amaurosis Fugax
 * Vertebrobasilar Artery Insufficiency

Amaurosis Fugax

 * Unilateral
 * Shade coming down over vision, dimming of vision, or total loss of vision lasting 2-30 minutes and then completely resolves
 * Carotid artery or cardiac emboli
 * Major cause of death is coronary disease
 * Work up: carotid US, echo, query for symptoms of and consider lab work-up for Temporal Arteritis.

Vertebrobasilar Artery Insufficiency

 * Bilateral episodes of decreased vision, blurring, or dimming of vision, lasting seconds to minutes
 * Other symptoms: ataxia, vertigo, transient dysarthria or dysphagia, hemiparesis, hemisensory disturbances
 * Caused by atheromatous occlusion, HTN, microembolization, fluctuations in CO
 * Much less likely to find a treatable structural vascular abnormality compared with carotid disease
 * Antiplatelet or anticoagulant therapy

Angle-Closure Glaucoma
=Links & References=
 * Hyperopia, antatomically shallow anterior chamber
 * As the lens grows, anterior chamber shallows
 * The angle closure mostly occurs in those over 50
 * Patient has severe eye pain, redness, HAs, nausea, photophobia, decreased vision, and halos
 * Pupil is mid-dilated and poorly reactive
 * Treat with diamox, glaucoma eye drops to decrease intraocular pressure and give peripheral laser iridotomy ASAP