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

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. EXAMINAT
ION
•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

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

14. 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: ♀ > ♂

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

16. 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

17. 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

18. 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

19. 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

20. 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%)

21. 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)

22. 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

23. CLINICAL FEATURES
•Painless central or pericentral
visual impairment
•Metamorphopsia
•Scotoma

24. 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

25. 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).

26. 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.

27. CLINICAL FEATURES
•Generally bilateral,
progressive visual field loss (from
peripheral to central)
•Halos around lights may occur.
•cupping and pallor of optic disc

28. 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

29. 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.

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

31. •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.

32. 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.

33. 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

34. 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

37. 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.

39. 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

40. 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)

41. 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

42. 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.

43. DIAGNOSTICS
 Perimetry
Measurement of the patient's field of
vision

44. •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

45. 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

46. 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

47. 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)

49. CASE STUDY