Chronic visual loss

Chronic Visual Disturbance

& Visual Loss

Dr. Riyad Banayot

Basic Anatomy

Diagnosis is based on

History: Gradual : Sudden Painless: Painful Unilateral : Bilateral Transient : Permanent

Examination: VA Slit lamp Dilated fundus

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)

RememberSometimes, chronic visual loss in ONE

eye, noted incidentally, by occluding the normal eye:

CHRONIC LOSS OF VISION CAN PRESENT ACUTELY!!

Tear Film

Dry Eye: decreased production or increased evaporation

Affect Quality of vision because of associated irregularity of tear film and optical refracting surface

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)

Corneal Causes

Refractive errors Myopia Hypermetropia Astigmatism

DystrophyScarringEdema

Refractive error

Corrected with pinhole Management:

• Glasses• Contact lenses• Refractive surgery

If not corrected in childhood leads to Amblyopia

Presbyopia

Corneal Dystrophies

- Rare inherited disorders

- Progressive, usually bilateral

- Affect transparency

Lattice

Granular

Macular

Keratoconus

Treatment options: Glasses Contact lens Crosslinking PK

Corneal Scarring

Multiple causes: Trauma Infectious (eg., herpes) Post-surgical

Corneal Edema

Mostly caused by dysfunction of the

corneal endothelium:- Hypotony- Dystrophy- Trauma- Infectious (e.g. herpes)- Post-surgical

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)

Lens-related Causes (cataract)

Opacification of the transparent clear structure

Age-related NS Myopic shift

Traumatic(Penetration, concussion, radiation)

Steroid induced Systemic or topical

Types

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

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

ON changes

C/D: 0.6

Rim loss

NFL loss

Disc hge.

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

Treatment options

Goal is to stabilize the IOP to protect the optic nerve against further damage

Options: Drops Laser Surgery

Glaucoma - Medications Decrease aqueous production:

• Beta blockers: Timolol• Alpha agonists: Brimonidine• Carbonic anhydrase inhibitors: Diamox

Increase aqueous outflow:• Miotics: Pilocarpine• Epinephrine• Prostaglandin analogs: Latanoprost

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

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)

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

Diabetes Mellitus Diabetic retinopathy Diabetic macular edema

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

Vascular Insufficiency

Arterial occlusions (CRAO, BRAO) Venous occlusions (CRVO, BRVO)

Arterial occlusions

CRAO Sudden and profound

loss of vision EMERGENCY

BRAO Altitudinal or

sectoral visual field loss

cherry-red spot

Venous occlusions

CRVOSudden loss of visionseverity 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

Ocular tumors Ciliary body:

• Melanoma choroid:

• Melanoma• Hemangioma• Metastases

Primary ocular lymphoma Retina and optic nerve:

• Retinoblastoma• Astrocytoma• Hemangioma

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

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

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

Macula

1.5 mm in diameter Central vision: BEST VISUAL ACUITY Color vision

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)

Macular DegenerationDry 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

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, …?

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)

OPTIC NERVE

1.2 million cells 80 % visual fibers 20 % pupillary fibers

Carries visual information from the eye to the brain

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

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

Drug Toxicity

Excessive Alcohol Smoking Chloroquine (malaria) Chloropromazine (pschosis) Steroids Ethambutol (TB)

Amiodarone Tetracycline, Vitamin A (BIH)

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

Thank you for your attention