Dr Amani Badawi ASSISTANT PROFESSOR OPHTHALMOLOGY Visual loss Dr Amani Badawi ASSISTANT PROFESSOR OPHTHALMOLOGY Amani Badawi 4/23/2017

Acute Visual Loss

Acute visual loss

History Examination Age POH & PMH Onset Duration Severity of visual loss compared to baseline Monocular vs. binocular ? Any associated symptoms Visual acuity assessment Visual fields Pupillary reactions Penlight or slit lamp examination Intraocular pressure Ophthalomoscopy - red reflex - assessment of clarity of media - direct inspection of the fundus

1-Central Retinal Artery Occlusion (CRAO) True ophthalmic emergency! Sudden painless and often severe visual loss Permanent damage to the ganglion cells caused by prolonged interruption of retinal arterial blood flow Characteristic “ cherry-red spot ” Months later, pale disc (optic atrophy) due to death of ganglion cells and their axons

1-Central Retinal Artery Occlusion (CRAO) treatment As before + Ocular massage: -To dislodge a small embolus in CRA and restore circulation -Pressing firmly for 10 seconds and then releasing for 10 seconds over a period of ~ 5 minutes Ocular hypotensives, vasodilators, paracentesis of anterior chamber

2-Branch Retinal Artery Occlusion (BRAO) Sector of the retina is opacified and vision is partially lost Most often due to embolus Treat as CRAO

3-Central Retinal Vein Occlusion (CRVO) Acute loss of vision Disc swelling, venous engorgement, cotton-wool spots and diffuse retinal hemorrhage. Needs medical evaluation Long term complication: neovascular glaucoma, and macular edema so periodic ophthalmic follow up

4-Optic Nerve Disease Non-Arteritic Ischemic Optic Neuropathy (NAION) - vascular disorder  pale, swollen disc +/- splinter hemorrhage  loss of VA , VF ( often altitudinal ) Treatment : systemic steroids

4-Optic Nerve Disease Optic neuritis - idiopathic or associated with multiple sclerosis - young adults - Unilateral decreased visual acuity and colour vision -RAPD -pain with ocular movement -bulbar (disc swelling) or retrobulbar (normal disc)

5-Retinal Detachment Retinal detachment - flashes, floaters, shade over vision - elevated retina +/- folds Macular disease - decrease central vision - metamorphopsia

Separation of sensory retina from RPE by subretinal fluid (SRF) Rhegmatogenous - caused by a retinal break Non-rhegmatogenous - tractional or exudative Amani Badawi

6-Trauma Trauma

Hyphema

Ruptured globe Open globe should be suspected in any patient who has a history of trauma to the eye, especially with a laceration or puncture wound that extends through the eyelid, followed by pain and decreased visual acuity &hyptony.

Anterior segment complications of blunt trauma Hyphaema Vossius ring Sphincter tear Iridodialysis Cataract Lens subluxation Angle recession Rupture of globe Amani Badawi

Posterior segment complications of blunt trauma Choroidal rupture and haemorrhage Avulsion of vitreous base and retinal dialysis Commotio retinae RD Macular hole Optic neuropathy

Complications of penetrating trauma Flat anterior chamber Uveal prolapse Damage to lens and iris Amani Badawi Vitreous haemorrhage Tractional retinal detachment Endophthalmitis

7-Media Opacities Corneal edema: Corneal abrasion &ulcer - ground glass appearance - as in acute congestive glaucoma Corneal abrasion &ulcer Vitreous hemorrhage - traumatic - retinal neovascularization

8-Endophthalmitis Background: Bacterial endophthalmitis is an inflammatory reaction of the intraocular fluids or tissues caused by microbial organisms.

History Exogenous Endogenous Classification is based on routes of entry. Exogenous Endogenous

Physical Visual acuity decreased below the level expected Lid edema General findings Visual acuity decreased below the level expected Lid edema Conjunctival hyperemia Corneal edema Anterior chamber cells and flare &Hypopyon Vitritis Loss of red reflex Retinal periphlebitis if view of fundus possible

9-Visual Pathway Disorders Hemianopia - Causes: vascular or tumors -Types Cortical Blindness - Extensive bilateral damage to cerebral pathways - Normal pupillary reactions and fundi

Chronic Visual Loss

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 PHx: HTN, T2DM diet controlled O/E: VA R 6/18 and L 6/12

Case 1 What is the likely diagnosis?

1-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

Case 2 A 76 year old man has noted visual distortion 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

Case 2

Case 2

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

Geographic atrophy – dry AMD RPE atrophy – demarcated pale area, visible underlying choroidal vessels 34

Choroidal neovascularisation – wet AMD OCT – RPE thickening, pre-retinal hemorrhage & elevation of retina 35

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 =CNV Observation Laser photocoagulation Photodynamic therapy (PDT) Intra-vitreal injection of Anti-VEGF

Anti-VEGF therapies VEGF-A stimulates angiogenesis and vascular permeability Intravitreal injection of monoclonal antibodies Ranibizumab (Lucentis) Off-label Bevacizumab (Avastin)

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 Right eye

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

Case 3 LE RE 1. generalised/focal enlargement of the cup 2. thinning of neuroretinal rim 3. asymmetry of cupping between patient’s eyes 4. Disc hemorrhage 5. parapapillary atrophy (more common inglaucomatous eyes). 42

3-Glaucoma 1. Optic nerve damage (optic disc cupping) 2. Increased IOP Increased Cup:disc ratio Loss of neuroretinal rim 2. Increased IOP 3. Peripheral visual defects IOP: 1. vascular dysfunction 2. mechanical compression 43

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 Secondary Congenital 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 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 : Yag laser AC  under conjunctiva, bleb 49

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?

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

Case 5 – spot diagnosis

5-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, …? Pallor of optic nerve head, attenuation of retinal vessels, cellophane maculopathy, CME, PSC 53

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

Diabetic retinopathy Microaneurysms Dot & blot hemorrhages Circinate exudate – retinal degeneration CSME 55

Diabetic retinopathy Cotton-wool spots – area of ischemia 56

Diabetic retinopathy Venous tortuosity – IRMA (intra-retinal microvascular abnormalities) 57

Diabetic retinopathy neovascularisation 58

Diabetic retinopathy Neovascularisation of disc 59

Diabetic retinopathy Focal diabetic maculopathy – amenable to focal photocoagulation, good prognosis 60

Diabetic retinopathy Diffuse exudative maculopathy – amenable to grid photocoagulation, guarded prognosis 61

Diabetic retinopathy Ischaemic maculopathy – not amenable to laser 62

Diabetic retinopathy Vitreal hemorrhage and retinal detachment 63

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

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