Gradual vision loss

clinical approach to gradual vision loss

1. Gradual vision loss By Ali jafaar alkhafajy

2. Objectives -general aspects of gradual vision loss - epidemiology and etiology - clinical approach to patient with gradual vision loss - Clinical conditions associated with gradual vision loss

3. Introduction -chronic , slowly progressive loss of vision -Chronic loss of vision is almost always painless  - Visual loss is usually bilateral, but may occur asymmetrically -happens over weeks to years rather than minutes , hours or a few days

4. definitions blindness is defined as visual acuity worse than 3/60 in both eyes, or a visual field restricted to less than 10 degrees around central fixation bilaterally. Visual impairment is divided into different categories, but generally refers to visual acuity worse than 6/18 in the better eye

5. Epidemiology -Gender Female > Male -Age 82% in patients > 50 years old - Gradual vision loss is more common than acute

6. Approach to vision loss History Age : Degenerative and vascular disorders seen in adults Neoplasms/ tumor types are age dependent Sex: Optic neuritis and giant cell arteritis are more prevalent in females

7. Is the visual loss monocular/ binocular ? Monocular vision loss : abnormality in the eye itself or in the optic nerve anterior to the chiasm Binocular vision loss result from bilateral anterior lesions or more likely chiasmal / retrochiasmal lesion How quickly the vision become blurry? What is the pattern and degree of vision loss ? History of previous ocular disease? History

8. Present medications, ocular and systemic? Diabetes and hypertension ? positive family history of  glaucoma? any other changes to your vision? ( floaters, flashes, distortion, progressive myopia, glare) Are your eyes affected in any other way ? ( Pain, photophobia, and redness) Do you have any symptoms elsewhere? (temporal headache, pain on chewing, fatigue, fever-like symptoms, and myalgia) History

9. Examination Visual acuity Improvement in the visual acuity when a pin hole is used suggests a refractive cause of visual loss . Cornea and conjunctiva Conjunctival redness → conjunctivitis and iritis, rather than cataract new corneal opacity suggests an infective lesion . use fluorescein stain to highlight corneal epithelial damage. Red reflex Opacities within the  red reflex , darkening of the red reflex, or obscuration of ocular fundus detail during ophthalmoscopy  

10. Examination Pupils check the direct and consensual pupil responses Swinging light reflex → If a relative afferent pupillary defect is present, suggesting optic nerve disease. Lens cataract usually appears as whiteness in the pupil Retinal examination If the disc looks pale or cupped → glaucoma or optic nerve disease. Haemorrhages in the central retina → wet macular degeneration. Scattered haemorrhages associated with yellow exudates → retinal vein occlusion or diabetic retinopathy. Tonometry

11. Etiology

12. Percentage of blindness by cause for all ages in 2015

13. cataract Cataract is a condition characterized by clouding of the lens of the eye . Leading cause of visual impairment and blindness in the world Prevalence  of acquired  cataracts Increases with age 40–80 years: ∼ 17.5 % > 80 years: ∼70 % Sex: ♀ > ♂

14. etiology  may be congenital or acquired . Congenital cataracts (< 1%) Hereditary congenital cataracts congenital infections (rubella, hepatitis, mumps, toxoplasmosis) Galactosemia

15. etiology Acquired cataracts (> 99 %) Age-related  (> 90%) Associated with comorbidities/syndromes Diabetes mellitus Galactosemia Drug-induced Glucocorticoids Trauma (traumatic cataract) Physically related conditions Radiation Excessive sunlight or UVB exposure

16. clinical features Reduced visual acuity : blurred, clouded, or dim vision impairment of vision is usually  painless  and often bilateral Glare in daylight, in low sunlight ,   associated with halos around lights Grey , white, yellow, or brownish  clouding  of the  lens

17. Refractive error ( Ametropia ) Mismatch between axial length and refractive power. Parallel light rays don’t fall on the retina (no accommodation) Types:- Nearsightedness (Myopia ) Farsightedness (Hyperopia) Astigmatism Presbyopia

18. Age-related macular degeneration Age-related macular degeneration (AMD) is a degenerative disease of the  retina that may result in blurred or no vision in the center of the visual field . AMD is the leading cause of blindness in individuals > 65 years in developed countries Risk factors Advanced   age Family history and genetic predisposition  Cardiovascular disease  Smoking  Obesity

19. Pathophysiology AMD is characterized by progressive degenerative changes in the  central part of the  retina ( macula ) → visual impairment . Types :- Dry AMD  (∼ 90 %) Wet AMD  (∼ 10%)

20. Dry AMD  deposition of yellow-whitish material ( drusen ) in and under the  retinal pigment epithelium   → slow progressive atrophy of the local retinal pigment epithelium  impairment ( usually over decades ) 

21. Wet AMD choroidal  neovascularization →  leaking of intravascular serous fluid and blood (between the retinal pigment epithelium and Bruch's membrane) →   sudden  localized elevation of the  macula and/or detachment of the  retinal  pigment  epithelium

22. Clinical features Painless central or pericentral visual impairment Metamorphopsia   Scotoma 

23. Treatment of AMD No causal treatment available Wet AMD First-line :  injection of VEGF inhibitors   ( eg . ranibizumab ) into the vitreous body Second-line: when VEGF is contraindicated Laser coagulation: direct thermal coagulation of neovascularization Photodynamic therapy : intravenously administered dye is activated in the eye by laser light → local toxic effect → thrombosis of subretinal neovascularizations

24. Glaucoma Glaucoma  is a group of eye diseases which result in damage to the optic nerve and cause vision loss .   The two main types of glaucoma are : Open-angle glaucoma Most common type of glucoma develops slowly over time and there is no pain. Angle-closure glaucoma This is a less common type of glaucoma  can be either:- chronic (an anatomically narrow angle or temporary episodes of angle closures over time) or acute (the angle narrows or closes suddenly).

25. Pathophysiology of open-angle glaucoma Secondary clogging of the trabecular meshwork or reduced drainage  →   gradual  ↑ in  IOP → vascular compression  → ischemia to the optic nerve  → progressive visual impairment.

26. Clinical features Generally  bilateral, progressive visual field loss  (from peripheral to central)  Halos around lights may occur . cupping  and pallor of optic disc

27. Treatment of open-angle glaucoma   Improve drainage: First-line :  Topical prostaglandins  (e.g.,  latanoprost ) Adverse effects: epithelial keratopathy, iris hyperpigmentation, eyelash thickening and lengthening Reduce aqueous humor  production: Topical beta blockers (e.g.,  timolol ) α2 agonists (e.g.,  apraclonidine ) Alternative first-line treatment:  laser trabeculoplasty   Refractory cases: surgical trabeculectomy

28. Corneal blindness Scarring of the cornea caused by a wide variety of infectious and inflammatory diseases leads to severe vision loss and blindness . Trachoma is one of the main causes of corneal scarring and is responsible for blindness or visual impairment in nearly 2.0 million individuals .

29. etiology Infections and Ulcerations : (Bacterial , fungal, or viral keratitis ) Eye trauma (chemical , thermal , open-globe ) Vitamin A deficiency Hereditary dystrophies Fuch’s Endothelial Dystrophy

30. Corneal opacification is usually easily diagnosed by the presence of a reduction in the red reflex, with underlying iris details not being clear in the area of opacification. corneal grafting is needed to remove the opacified , scarred corneal tissue and to restore vision.

31. Diabetic retinopathy Epidemiology After  15 years with DM,  approx. 90% of type 1 diabetic patients And 25 % of type 2 diabetic patients develop diabetic retinopathy .

32. Clinical features  asymptomatic until very late stages of disease Visual impairment Progression to blindness classification of diabetic retinopathy Nonproliferative retinopathy : accounts for most cases  Proliferative retinopathy

33. Nonproliferative retinopathy Fundoscopic Findings: intraretinal microvascular abnormalities, including:- Microaneurysms caliber changes in venous vessels intraretinal haemorrhage hard exudates retinal edema and cotton-wool spots Visual loss, most commonly due to macular edema

34. Proliferative retinopathy Fudoscopic Findings :  Preretinal  neovascularization is the hallmark of   PDR   fibrovascular   proliferation  vitreous haemorrhage traction retinal detachment    rubeosis iridis   → secondary glaucoma. findings  of  nonproliferative retinopathy are usually present. Visual loss may be due to vitreous hemorrhage ,  retinal detachment, or  neovascular glaucoma.

35. Treatment Nonproliferative retinopathy Laser treatment: focal photocoagulation Intravitreal  anti-vascular endothelial growth factor (VEGF) injection Proliferative retinopathy and severe  nonproliferative retinopathy Laser treatment:  panretinal photocoagulation Vitrectomy  in case of traction retinal detachment and vitreal hemorrhage

36. Retinitis pigmentosa Definition: progressive hereditary dystrophy of the retina or of the photoreceptors and the retinal pigment epithelium Epidemiology: early onset (5–30 years) Etiology Hereditary or spontaneous mutations (> 45 genes are known as triggers; e.g., mutations in the rhodopsin gene )

37. Clinical features Night blindness Narrowing field of vision (ring-shaped area of blindness) Glare sensitivity Defects in the perception of contrast and colour In early stages: good central vision In advanced stages: loss of vision

38. Diagnostics Ophthalmoscopy Pattern of dark spots and star-shaped spots that develop from the periphery to the center of the retina Electroretinography measures the electrical responses of various cell types in the retina, including the photoreceptors, inner retinal cells, and the ganglion cells. 

39. Diagnostics Perimetry Measurement of the patient's field of vision

40. Differential diagnosis : Drugs ( phenothiazines , chloroquine) may induce similar symptoms to those of retinitis pigmentosa → pseudoretinitis pigmentosa Treatment : No effective treatment is known. Prognosis: often leads to blindness

41. Compressive Optic Neuropathy caused by injury to the optic nerve by an extrinsic lesion . Optic nerve compression by an extrinsic lesion cause atrophy of ganglion cell axons either through ischemia or mechanical disruption of axonal transport . Rarely, an intrinsic lesion of the optic nerve ( ie , optic nerve glioma) can cause damage to the individual axons due to slow compression of the fascicles within the tumor . Compressive optic neuropathy (CON) is relatively rare

42. Etiology Most common causes: optic neuritis, glaucoma Vascular  E.g., central retinal artery occlusion orbital/intracranial lesion Hydrocephalus Hereditary: E.g. autosomal-dominant  optic atrophy

43. Clinical features slowly progressive or chronic vision loss in one or both eyes . Bilateral cases can result from midline lesions ( eg , pituitary adenoma, craniopharyngioma , meningioma) or from bilateral lesions ( eg , thyroid eye disease ). blurred vision dimness of vision color blindness   visual field defects (e.g., central scotoma)

44. Case study