Chronic Visual Loss Emil Kurniawan SHMO Royal Melbourne Hospital

Case 1 A 75 year old woman is seen for an annual physical examination and complains of mild difficulty in reading and seeing street signs Vision is especially worse at night, and now has trouble with her knitting PHx: HTN, T2DM diet controlled, ex-smoker O/E: VA R 6/18 and L 6/12

Case 1 What is the likely diagnosis?

Cataract Symptoms gradual over years 1. Reduction in visual acuity Worsening of existing myopia Correction of hyperopia “second sight of the aged” 2. Loss of contrast sensitivity in low light 3. Glare in bright light Forward scatter of light

Pathophysiology Loss of organisation of proteins in lens Progressive opacity Symptoms due to blockage, aberrant refraction or forward reflection of light

Causes Age-related by far the most common Multifactorial Environmental factors (UV, radiation, toxins…) Diabetes, hypertension, obesity, smoking, … Ocular: high myopia, uveitis Steroids Trauma Syndromic

Types

Management Surgery Timing and indication of surgery Driving GA, LA, topical Importance of complete ophthalmological assessment Post-op follow-up: 1 day, 1 week, 1 month

Management

Complications Intraoperative Posterior capsule rupture Expulsive (choroidal) hemorrhage Postoperative Endophthalmitis Cystoid macular edema Retinal detachment Posterior capsule opacification IOL dislocation

Case 2 A 76 year old man has noted visual distortion from the RE over the past week Straight lines viewed through his right eye dipped down in the centre Round plates seem to have “edges” O/E: VA R 6/18 and L 6/6 What is the likely diagnosis? What test are you going to do?

Case 2

Macular degeneration Loss of central vision Reading, recognising faces impaired Peripheral (navigational) vision preserved Leading cause of legal blindness in developed world Multifactorial Age Smoking, vascular disease, UV light, diet, FHx, … Atrophic (dry) or exudative (wet)

Macular degeneration Atrophic – 90% Drusen Geographic atrophy Photoreceptor degeneration Gradual over years Often asymptomatic More obvious scotoma when light adapting Exudative – 10% Choroidal (sub-retinal) neovascularisation Pre-retinal hemorrhage Elevation of retina Subretinal fibrosis Metamorphopsia Central scotoma Rapidly progressive (weeks)

Macular degeneration

Geographic atrophy – dry AMD

Choroidal neovascularisation – wet AMD

Macular scarring – wet AMD

Management – dry AMD Lifestyle Stop smoking, reduce UV exposure, Zinc & antioxidants Low vision aids Legal blindness and driving Monitoring with Amsler chart

Management – wet AMD Observation Laser photocoagulation Indication: well-demarcated CNV Best for extrafoveal lesions (MPS study) Induce scotoma, recurrence, complications Verteporfin photodynamic therapy (PDT) Photosensitizer activated with low light Recurrence, needs re-treatment every 3 months Anti-VEGF

Anti-VEGF therapies VEGF-A stimulates angiogenesis and vascular permeability Intravitreal injection of monoclonal antibodies Ranibizumab (Lucentis) MARINA and ANCHOR studies Off-label Bevacizumab (Avastin) SANA and CATT trials Combination with other therapy modalities not useful Future: silencer RNAs – bevasiranib, …

Case 3 A 68 year old man was referred from his optometrist for visual field testing He has not reported any problems with vision, but the test report shows a reduction in peripheral vision in the RE

Case 3 What is your likely diagnosis? What further examination are you going to do?

Case 3 LE RE

Glaucoma 1. Optic nerve damage (optic disc cupping) Cup:disc ratio >0.6 Loss of neuroretinal rim 2. Increased IOP 3. Peripheral visual defects (navigational sight)

The trick of IOP Only 10% with IOP>21 have glaucoma The rest have ocular hypertension Only 50% of glaucoma patients have IOP>21 The rest have normal tension glaucoma

Glaucoma Types Primary Open angle (90%) Closed angle Secondary Congenital

Primary open angle glaucoma “The silent thief of sight” Asymptomatic Usually detected on routine examination Risk factors: IOP, age, FHx, DM, myopia Impaired drainage of aqueous humor through trabecular meshwork Due to age-related morphological changes

Primary open angle glaucoma

Management Aim to stop progress Cannot recover sight already lost Medical – reduction of aqueous secretion Beta-blockers (Timolol) Alpha-agonists (Brimonidine) Prostaglandin analogues (Latanoprost) Parasympathomimetics (Pilocarpine) Carbonic anhydrase inhibitors (Brinzolamide)

Management Surgical Argon and selective laser trabeculoplasty Filtering surgery Trabeculectomy Laser peripheral iridotomy Iridectomy Canaloplasty

Case 4 A 13 year old girl is seen for physical examination at school. She admits to difficulty in reading the blackboard, but not in reading textbooks. She does not wear glasses. O/E: VA R 6/36 ph 6/6 and L 6/36 ph 6/6 What is your diagnosis?

Refractive error Corrects with pinhole Management: glasses, contact lenses, refractive surgery

Case 5 – spot diagnosis

Retinitis pigmentosa Genetically inherited Progressive retinal dystrophy Night blindness, tunnel vision, legal blindness Bony spicules from mottling of RPE Incurable Future: gene therapy, bionic eye, …?

Case 6 – diabetic retinopathy Microvascular retinal changes Blindness is progressive, but preventable Annual retinal examination Tight T2DM control HbA1c 6-7% Appropriate laser treatment Pre-proliferative retinopathy Proliferative retinopathy Also predisposes to cataract & glaucoma

Diabetic retinopathy

Summary Causes of chronic visual loss Cataract Glaucoma Age-related macular degeneration Refractive error Retinitis pigmentosa Diabetic retinopathy