Causes of chronic visual loss: pre-retinal, retinal and post-retinal

1. Chronic
Visual Disturbance
& Visual Loss
Dr. Riyad Banayot

2. Basic Anatomy

3. Diagnosis is based on
 History:
 Gradual : Sudden
 Painless: Painful
 Unilateral : Bilateral
 Transient : Permanent
 Examination:
 VA
 Slit lamp
 Dilated fundus

4. Where is the problem?
 Pre-retinal:
 Tear film
 Cornea (Refractive error, dystrophy, KC, scarring, edema)
 Lens (age-related, traumatic, steroid-induced)
 Glaucoma
 Retinal:
 DM (diabetic retinopathy, macular edema)
 Vascular insufficiency (arterial or venous occlusion)
 Tumors
 Macular degeneration
 Post-retinal:
 Anterior to optic chiasm (if optic nerve = monocular)
• Compressive optic neuropathy (intracranial masses, thyroid eye disease)
• Toxic/nutritional (nutritional deficiencies, alcohol/tobacco amblyopia)
 Optic chiasm lesions (pituitary adenoma)

5. Remember
Sometimes, chronic visual loss in ONE
eye, noted incidentally, by occluding
the normal eye:
CHRONIC LOSS OF VISION CAN
PRESENT ACUTELY!!

6. Tear Film
 Dry Eye: decreased
production or
increased evaporation
 Affect Quality of
vision because of
associated irregularity
of tear film and optical
refracting surface

7. The Cornea
 Allows light to enter
the eye & provides
most of the eye’s
optical power
 -0.5-0.8 mm thick
 -Transparent due to
its uniformity,
avascularity and
deturgescence (relative
dehydration)

8. Corneal Causes
Refractive errors
 Myopia
 Hypermetropia
 Astigmatism
Dystrophy
Scarring
Edema

9. Refractive error
 Corrected with pinhole
 Management:
• Glasses
• Contact lenses
• Refractive surgery
 If not corrected in childhood leads to
Amblyopia
 Presbyopia

10. Corneal Dystrophies
- Rare inherited disorders
- Progressive, usually bilateral
- Affect transparency

11. Lattice
Granular
Macular

12. Keratoconus
Treatment options:
 Glasses
 Contact lens
 Crosslinking
 PK

13. Corneal Scarring
 Multiple causes:
 Trauma
 Infectious (eg., herpes)
 Post-surgical

14. Corneal Edema
 Mostly caused by dysfunction of the
corneal endothelium:
- Hypotony
- Dystrophy
- Trauma
- Infectious (e.g. herpes)
- Post-surgical

15. The Lens
 Biconvex, avascular,
transparent structure
 Sits inside a thin
capsule, attached to the
ciliary body by the
zonules
 Provides the remainder
of the eye’s optical
power (along with the
cornea)

16. Lens-related Causes
(cataract)
Opacification of the transparent clear structure
 Age-related
 NS
 Myopic shift
 Traumatic
(Penetration, concussion, radiation)
 Steroid induced
 Systemic or topical

17. Types

18. Glaucoma
 A group of diseases that have in common
a characteristic optic neuropathy with
associated visual function loss
 Elevated (IOP) is one of the primary risk
factors (its presence or absence does not
have a role in disease definition)
 if left untreated, glaucoma can lead to
permanent damage to the optic nerve
and resultant visual field loss
 Can progress to blindness

19. Glaucoma
 Primary: Open-angle, angle-closure
 Secondary: Inflammatory, traumatic,
neovascular, steroid-induced etc…
 Congenital
 Often asymptomatic
 Constriction of VF
 High IOP, can have blurry vision and halos around
lights

20. ON changes
 C/D: 0.6
 Rim loss
 NFL loss
 Disc hge.

22. Primary Open Angle
Glaucoma
 Most common (90%)
 Usually bilateral (can be asymmetric)
 Prevalence increases with age
 Angle is open, eye is quiet
 Increased resistance to aqueous drainage
at the level of the trabecular meshwork is
thought to be the main pathophysiologic
feature

24. Treatment options
 Goal is to stabilize the IOP to protect the
optic nerve against further damage
 Options:
 Drops
 Laser
 Surgery

25. Glaucoma - Medications
 Decrease aqueous production:
• Beta blockers: Timolol
• Alpha agonists: Brimonidine
• Carbonic anhydrase inhibitors: Diamox
 Increase aqueous outflow:
• Miotics: Pilocarpine
• Epinephrine
• Prostaglandin analogs: Latanoprost

26. Glaucoma – Lasers & Surgery
 Lasers:
 Usually when medical management fail
• ALT & SLT: for OAG
• Peripheral iridotomy: for ACG
 Surgery:
 usually when medical management and laser
treatments fail
• Trabeculectomy: sub-conjunctival shunt of
aqueous
• Drainage devices (valves)
• Cyclodestruction: last resort – destruction of
ciliary body

27. Where is the problem?
 Pre-retinal:
 Tear film
 Cornea (Refractive error, dystrophy, KC, scarring, edema)
 Lens (age-related, traumatic, steroid-induced)
 Glaucoma
 Retinal:
 DM (diabetic retinopathy, macular edema)
 Vascular insufficiency (arterial or venous occlusion)
 Tumors
 Macular degeneration
 Post-retinal:
 Anterior to optic chiasm (if optic nerve = monocular)
• Compressive optic neuropathy (intracranial masses, thyroid eye disease)
• Toxic/nutritional (nutritional deficiencies, alcohol/tobacco amblyopia)
 Optic chiasm lesions (pituitary adenoma)

28. Retina
 Neural tissue lining
the inside of the eye
 Converts the visual
image into a
neurochemical
message and sends it
to the brain
 Is made up of 10
anatomic layers

29. Diabetes Mellitus
 Diabetic retinopathy
 Diabetic macular edema

30. Diabetic Retinopathy: Risk Factors
 Duration of diabetes: most important risk
factor
 Poor metabolic control
 Pregnancy: can be associated with rapid
progression
 HTN
 Nephropathy
 Smoking
 Obesity
 Hyperlipidemia

31. Vascular Insufficiency
 Arterial occlusions (CRAO, BRAO)
 Venous occlusions (CRVO, BRVO)

32. Arterial occlusions
 CRAO
 Sudden and profound
loss of vision
 EMERGENCY
 BRAO
 Altitudinal or
sectoral visual field
loss
cherry-red spot

33. Venous occlusions
 CRVO
Sudden loss of vision
severity of symptoms:
Non-ischemic: 75%
Ischemic
Characteristic finding:
Retinal hemorrhages
 BRVO
 Visual loss &
prognosis depends on
the amount of macular
drainage compromised
by the occlusion

34. Ocular tumors
 Ciliary body:
• Melanoma
 choroid:
• Melanoma
• Hemangioma
• Metastases
 Primary ocular lymphoma
 Retina and optic nerve:
• Retinoblastoma
• Astrocytoma
• Hemangioma

35. Choroidal Melanoma
 Most common primary intraocular tumor in
adults
 Presentation usually in 6th decade:
 Asymptomatic vs. visual field defect and/or
decreased visual acuity
 Raised, usually pigmented lesion visible at the
back of the eye

36. Choroidal Metastases
 usually present with visual impairment only
IF tumour is near the macula
 fast-growing, creamy colored lesion in
posterior pole
 Mets TO the choroid: most frequently from
bronchus in both sexes and the breast in
women

37. Retinoblastoma
 Most common malignant tumor of the eye
in childhood (1:20 000)
 Presentation:
 Mean age: 8 M (inherited), 25 M (sporadic)
 60% present with leukocoria
 Strabismus (20%)
 Malignant transformation of
primitive retinal cells

38. Macula
 1.5 mm in diameter
 Central vision: BEST VISUAL ACUITY
 Color vision

39. Macular Degeneration
 Progressive destruction of the macula
 Most common cause of irreversible visual loss in
the developed world
 Forms:
 Non-exudative (dry)
 Exudative (wet)
 Symptoms:
 Distorted vision (metamorphopsia)
 reduction (micropsia) or enlargement (macropsia) of
objects
 VF loss (scotoma)

40. Macular Degeneration
Dry Wet
Drusen (lipid products under
retina). No Rx
New vessels from the choroid grow into
the sub-retinal space; forming a SRNM &
hemorrhage into the sub-retinal space or
even through the retina into the vitreous.
Rx: injections

41. 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, …?

42. Where is the problem?
 Pre-retinal:
 Tear film
 Cornea (Refractive error, dystrophy, KC, scarring, edema)
 Lens (age-related, traumatic, steroid-induced)
 Glaucoma
 Retinal:
 DM (diabetic retinopathy, macular edema)
 Vascular insufficiency (arterial or venous occlusion)
 Tumors
 Macular degeneration
 Post-retinal:
 Anterior to optic chiasm (if optic nerve = monocular)
• Compressive optic neuropathy (intracranial masses, thyroid eye disease)
• Toxic/nutritional (nutritional deficiencies, alcohol/tobacco amblyopia)
 Optic chiasm lesions (pituitary adenoma)

43. OPTIC NERVE
 1.2 million cells
 80 % visual fibers
 20 % pupillary fibers
 Carries visual
information from
the eye to the brain

44. Compressive Optic Neuropathies
INTRACRANIAL MASSES:
 Optic nerve glioma
 Typically affects young women, end of first
decade
 Associated with NF-1
 Optic nerve sheath meningioma
 Most frequent in middle-aged women
 Unilateral, gradual visual impairment
 Any other orbital or chiasmal tumor compressing
any part of the optic nerve

45. Thyroid Eye Disease
 Autoimmune reaction causing inflammation of
EOMs. There is cellular infiltration associated
with increased secretion of glycosaminoglycan
and osmotic imbibition of water
 Vision loss from:
 Exposure Keratopathy
 Optic neuropathy
 Main findings:
 Soft tissue involvement & Restrictive myopathy
 Lid retraction
 Proptosis
 Optic neuropathy

46. Drug Toxicity
 Excessive Alcohol
 Smoking
 Chloroquine (malaria)
 Chloropromazine (pschosis)
 Steroids
 Ethambutol (TB)
 Amiodarone
 Tetracycline, Vitamin A (BIH)

47. Pituitary Adenoma
 Presentation usually in early adult life or
middle age
 symptoms:
 Visual symptoms: very gradual onset
• VF defect: usually, bitemporal hemianopia, worst in
the superior field, and extending inferiorly
• Color desaturation across vertical midline
• Optic atrophy: in 50% of cases with field defects
caused by pituitary lesions

48. Thank you for
your attention