visual loss compressed

Chronic Visual
Disturbance and Visual
Loss
Setareh Ziai
April 2nd, 2009
sziai@ottawahospital.on.ca

Where is the problem?
LMCC Objectives
 Pre-retinal:
 cornea (dystrophy, scarring, edema)
 lens (age-related, traumatic, steroid-induced)
 glaucoma
 Retinal:
 DM (diabetic retinopathy, macular edema)
 vascular insufficiency (arterial or venous occlusion)
 tumours
 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)

Where is the problem?
 Pre-retinal:
 cornea (dystrophy, scarring, edema)
 lens (age-related, traumatic, steroid-induced)
 glaucoma
 Retinal:
 DM (diabetic retinopathy, macular edema)
 vascular insufficiency (arterial or venous occlusion)
 tumours
 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)

Diagnosis based on:
- focused ophthalmological history
- monocular vs. binocular
- acute vs. chronic
- painful vs. painless
- exam: … start with gross examination
- VA
- slit lamp biomicroscopy +/- fluorescein
- dilated fundus examination
- VF testing
- fluorescein angiography +/- other tests

 **Remember for exam:
 sometimes, chronic visual loss in ONE eye is
noted incidentally some time later due to
occlusion of normal eye…: CHRONIC LOSS
OF VISION CAN PRESENT ACUTELY!!

Corneal Causes
- dystrophy
- scarring
- edema

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

Epithelium

Stroma

Endothelium

Corneal Dystrophies
- rare inherited disorders
- progressive, usually bilateral
- can affect any of the three layers of the
cornea
- affect transparency
- age at presentation: first to fourth decades

Corneal Dystrophies
- divided into:
- anterior dystrophies:
- epithelium
- may present with recurrent corneal erosions
- stromal dystrophies:
- usually present with visual loss
- if very anterior, can cause erosions and pain
- posterior dystrophies:
- endothelium
- vision loss secondary to edema (endothelial dysfx)

Corneal Scarring
- multiple causes:
- trauma
- infectious (eg., herpes)
- post-surgical

Corneal Edema
- most often caused by dysfunction of the
corneal endothelium:
- dystrophy
- trauma
- infectious (eg., herpes)
- post-surgical

If the corneal stroma opacifies due to
trauma or infection, or if there is
swelling or an irregularity of the
surface of the cornea, light cannot
properly reach the retina.

In some cases, a cornea from a
deceased donor can be transplanted.

Lens-Related Causes
(cataract)
- age-related
- traumatic
- steroid induced

The Lens
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)

 cataracts are due to the opacification of
this normally clear structure

Age-Related Cataract
- often affect the nucleus of the lens first:
- yellowing, followed by a browning of the lens
- eventually, liquefaction
- causes myopic changes (increased
refractive index of the lens)

Traumatic Cataract
- most common cause of unilateral cataract
in young individuals
- most often caused by direct penetrating
injury to the lens
- can also be caused by:
- concussion
- ionizing radiation to ocular tumours
- infrared radiation (glassblowers)

Steroid-Induced Cataract
- both systemic and topical steroids can be
the culprits
- posterior part of lens affected first
- children may be more susceptible
- if lens changes develop, dose should be
reduced to the minimum necessary
- early opacities may regress with
discontinuation of therapy

Glaucoma

 disease of the optic nerve, often
caused by an increase in intraocular
pressure due to poor drainage of
aqueous from the trabecular
meshwork…

Glaucoma

 if left untreated, glaucoma can lead to
permanent damage to the optic nerve
and resultant visual field loss
 can progress to blindness

Glaucoma

 by definition, glaucoma is a trimodal
disease, characterized by:

increased IOP
 optic nerve changes

 visual field changes

Goldmann Applanation Tonometer

Glaucoma
 classification:

 primary: open-angle, angle-closure
 secondary: inflammatory, traumatic,
neovascular, steroid-induced etc…
 congenital

Risk Factors for Glaucoma

 age
 african-american heritage
 high IOP
 family history
 myopia

Symptoms of Glaucoma

 often asymptomatic
 with late disease, constriction of
peripheral, and later central visual field
 with very high IOP, can have blurry
vision and halos around lights

Glaucoma: Optic Nerve
Changes
 increased cup:disc ratio
 thinning of neural rim
 progressive loss of nerve fiber layer
 flame hemorrhages on disc

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

 mechanism of action:
 decrease aqueous production:
• beta blockers: timolol
• alpha agonists: brimonidine
• carbonic anhydrase inhibitors: diamox
 increase aqueous outflow:
• miotics: pilocarpine
• epinephrine
• prostaglandin analogs: latanoprost

Glaucoma - Lasers

 usually when medical management
fails
 ALT (argon laser trabeculoplasty), SLT
(selective laser trabeculoplasty): for open
angle glaucomas
 peripheral iridotomy: for angle-closure
glaucomas
 high success rate

Glaucoma - 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

THE 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
- diabetic retinopathy
- diabetic macular edema

Diabetic Retinopathy
Ø microangiopathy
Ø affects pre-capillary arterioles, capillaries
and post-capillary venules
Ø features of:
l microvascular occlusion
l leakage
clinically, can be divided into:
l background DR (nonproliferative)
l preproliferative DR
l proliferative DR

Diabetic Retinopathy: Epidemiology
239 million people by 2010
doubling in prevalence since 1994
diabetes will affect:
28 million in western Europe
18.9 million in North America
138.2 million in Asia
1.3 million in Australasia

• #1 cause of blindness in patients 20-64 yrs
• prevalence increases with duration of diabetes and
patient age

rare to find DR in children < 10 yrs, regardless of duration
risk of developing DR increases after puberty

Epidemiology
Wisconsin Epidemiologic Study of Diabetic Retinopathy
l Between 1979-1980
l 1210 patients with Type 1
l 1780 patients with Type 2
l predominantly white population

l After 20 yrs, DR present in:
• 99% of Type 1
• 60% of Type 2

WESDR: Frequency of retinopathy in
subjects with type 1diabetes

WESDR: Frequency of retinopathy in
subjects with type 2 diabetes

Diabetic Retinopathy: Risk Factors
Ø duration of diabetes: most important risk
factor
Ø poor metabolic control
Ø pregnancy: can be associated with rapid
progression
Ø HTN
Ø nephropathy
Ø smoking
Ø obesity
Ø hyperlipidemia

Classification of Diabetic Retinopathy
Ø Classified into 2 stages

Nonproliferative Diabetic Retinopathy (NPDR)
early stage
also known as background DR (BDR)
further categorized based upon extent of DR
l mild, moderate, severe, very severe

l Proliferative Diabetic Retinopathy (PDR)
• more advanced stage

• ***Macular edema
• May be present at any stage of DR

NPDR
Ø typically asymptomatic
l fluctuating visual acuity:
• fluctuating blood sugar
l decreased visual acuity:
CSME
macular ischemia
review these patients annually

Proliferative Diabetic Retinopathy
Ø more likely to become
symptomatic than early
NPDR

Ø may have decreased
vision, sudden vision loss,
floaters, cobwebs, flashes,
dull eye ache

Ø PDR can also affect visual
function by affecting the
macula with resulting
macular ischemia and/or
edema

Proliferative DR
Ø affects 5-10% of the diabetic population
Ø neovascularization is the hallmark
l NVD: neovascularization of the disc

l NVE: neovascularization elsewhere

Ø new vessels are not only extremely fragile
(intraretinal or vitreous hemorrhage), but
often associated with fibrous proliferation,
leading to an increased risk of tractional retinal
detachment

Advanced PDR

 Tractional retinal
detachment
resulting from
contraction of
the fibrovascular
proliferative
tissue on the
retina

Panretinal Photocoagulation for High-risk
PDR
 goal is to induce
involution (or at
least arrest) of new
vessels by creating
areas of retinal
ischemia
 1200-3000 burns
 4 sessions

Vitrectomy for Vitreous
Hemorrhage / TRD

Diabetic Macular Edema (DME)
Ø retinal edema threatening or involving the
macula

diagnosis is made by slit-lamp exam,
confirmed by fluorescein angiography and/or
OCT

important observations include:
l location of retinal thickening relative to the

fovea
l presence and location of exudates

Treatment of CSME
 argon laser application

 intravitreal steroid injection

 intravitreal anti-VEGF injection

 pars plana vitrectomy

Ophthalmological Follow-Up
 Diabetic Screening

l Type 1 diabetics:
Dilated funduscopic exam (DFE) 5 yrs after
diagnosis
Newly diagnosed patients with Type 1 diabetes
rarely have retinopathy during the first 5 yrs

l Type 2 diabetics:
Type 2 diabetics typically diagnosed yrs after initial
onset
DFE at the time of diagnosis
Significant portion of newly diagnosed Type 2
diabetics have established DR at the time of
diagnosis

Vascular Insufficiency
- arterial occlusions (CRAO, BRAO)
- venous occlusions (CRVO, BRVO)

CRAO
 most of the retina is supplied by the
central retinal artery (branch of the
ophthalmic artery, which is the first branch
of the ICA)
 if this supply is interrupted (embolus,
thrombosis, inflammation, vasculitis or
compression), the retina becomes
ischemic
 irreversible damage occurs after
approximately 90 minutes

CRAO
 presentation is with sudden and
profound loss of vision
 RAPD is present
 orange reflex from the choroid stands
out at the fovea, and contrasts with the
surrounding pale retina (cherry-red
spot)
 must r/o temporal arteritis

CRAO
 most commonly the result of
atherosclerosis (thrombosis) but may
also be caused by calcific emboli
 often in older patients, with a hx of
arteriosclerosis
 may have had a hx of amaurosis fugax
(transient visual loss)

CRAO
 OPHTHALMOLOGIC EMERGENCY!!
 treatment:
 decrease IOP

 paracentesis

 ocular massage

 goal: to send the embolus distally
 **remember to r/o giant cell arteritis! (ESR, CRP, plt)
 poor prognosis: 60% < 20/400

BRAO
 sudden and profound altitudinal or
sectoral visual field loss
 similar causes as CRAO
 identify and treat associated medical
conditions (HTN, DM,
hypercholesterolemia, smoking,
vasculitis etc…)

BRAO
 retinal cloudiness in ischemic area
 +/- visible embolus
 also has a poor prognosis, unless the
obstruction can be dislodged within a
few hours

CRVO
 thrombosis of the central retinal vein
 sudden loss of vision in affected eye
 severity of symptoms varies…
 non-ischemic: 75%
 Ischemic
 most characteristic finding: retinal
hemorrhages

CRVO
 underlying associations
 advancing age
 systemic conditions: HTN, DM, smoking,
obesity, hyperlipidemia
 glaucoma
 inflammatory diseases: sarcoidosis, Behcet
disease
 thrombophilic disorders:
hyperhomocysteinaemia, antiphospholipid
antibody syndrome

CRVO
 Treatment:
 treat associated medical conditions
 decrease IOP if elevated
 pan-retinal photocoagulation
(laser) if:
• neovascularization (iris, angle,
retina)
• …especially if ischemic CRVO

BRVO
 thrombosis of a branch of the central
retinal vein
 visual loss depends on the amount of
macular drainage compromised by the
occlusion (peripheral occlusions may be
asymptomatic)
 characteristic findings in one sector of the
retina:
 dilatation and tortuosity of veins
 retinal hemorrhages
 retinal/macular edema


BRVO
 obstruction often at arterio-venous
crossings: arteries and veins share
adventitial sheath… thickening of the
arteriole (arteriosclerosis) compresses
the vein, eventually causing an occlusion
 often associated with:
 hypertension (75%)

 diabetes (10%)

BRVO
 prognosis: depends on amt of venous
drainage involved by the occlusion and
severity of macular ischemia: within 6 mos,
about 50% of eyes have a VA of 20/30 or
better
 main complications:
 chronic macular edema
 neovascularization
 laser photocoagulation may be helpful in
above cases

 ocular tumours:
 ciliary body:
• melanoma
 choroid:
• melanoma
• hemangioma
• metastases
 primary ocular lymphoma
 retina and optic nerve:
• retinoblastoma
• astrocytoma
• hemangioma

Choroidal Melanoma
 most common primary intraocular
tumour in adults
 presentation usually in 6th decade:
 asymptomatic vs. visual field defect and/or
decreased visual acuity
 signs:
 raised, usually pigmented lesion visible at

the back of the eye
 may be associated with retinal detachment

 optic nerve may be involved

Choroidal Melanoma
 treatment:
 consider size, location, activity of tumour,
state of fellow eye, general health/age of pt,
pt’s wishes/fears
• brachytherapy
• external radiotherapy
• transpupillary thermotherapy
• local resection
• enucleation
• exenteration
• palliative (may include chemo)

Choroidal Metastases
 …with choroidal melanoma, don’t forget
general medical investigations!
 mets TO the choroid:
• most frequently from bronchus in both sexes
and the breast in women, rarely kidney or GI
 CXR, rectal exam, mammography
 mets FROM the choroid:
• liver
 hepatic u/s, GGT, ALP
• lungs (rarely affected before liver)
 CXR

 usually present with visual impairment
only IF tumour is near the macula
 signs:
 fast-growing, creamy coloured lesion
 most often in posterior pole
 usually not very elevated (infiltrates laterally)

 treatment:
 observe: if asxic or receiving systemic chemo
 radiation: external beam or brachy
 transpupillary thermotherapy
 systemic therapy for the primary
 enucleation: for painful blind eye
 prognosis is poor…
 median survival: 8-12 mos for all pts, 15-17
mos for those with breast ca

Retinoblastoma
 most common malignant tumour of the eye
in childhood (1:20 000)
 mean age of presentation: 8 mos if
inherited, 25 mos if sporadic
 60% present with leukocoria (white pupillary
reflex)
 strabismus (20%)
 occasionally: painful, red eye
 if inherited: often bilateral

Retinoblastoma
 malignant transformation of primitive
retinal cells before their final differentiation

 can be caused by germinal mutations (can
be passed on to the next generation), or
can be sporadic (66% of cases)

Retinoblastoma
 this is a clinical diagnosis, but CSF and
bone marrow should be examined to check
for metastatic disease if ON involved or if
there is evidence of extraocular extension
 rx:
 small: cryotherapy, photocoagulation
 medium: brachytherapy, external beam, chemo
 large/advanced cases: chemoreduction + local
treatment, enucleation
 metastatic disease: chemo (intrathecal if cells
in CSF)

Retinoblastoma
 prognosis:
 depends on extent of disease at diagnosis
 overall mortality ~ 5-15%
 ~ 50% of children with the germinal mutation
will eventually develop a second primary
tumour (eg., osteosarcoma of the femur or
pinealoblastoma)

Macula
 1.5 mm in diameter
 central vision: BEST VISUAL ACUITY
 colour vision
 progressive destruction of the macular
area:
MACULAR DEGENERATION

Macular Degeneration
 most common cause of irreversible
visual loss in the developed world
 exists in two forms:
 non-exudative (dry) macular
degeneration
 exudative (wet) macular

degeneration

Non-exudative Macular
Degeneration
 lipid products arising from
photoreceptor outer segments are
found under retina
 can be seen with ophthalmoscope!
 called « drusen »

Exudative Macular
Degeneration
 new vessels from the choroid grow into
the sub-retinal space; form a sub-
retinal neovascular membrane

 subsequent hemorrhage into the sub-
retinal space or even through the retina
into the vitreous is associated with
profound loss of vision

 symptoms:
 since fovea is responsible for fine visual
resolution, any disruption will cause
severe visual impairment
• blurry/reduced vision
• distorted vision (metamorphopsia)
• reduction (micropsia) or enlargement
(macropsia) of objects
• VF loss (scotoma)

 rx:
 non-exudative (usually slowly
progressive):
• no actual medical treatment
• use low vision aids
• high dose antioxidants MAY be
beneficial (eg., vitalux)

 rx:
 exudative (can be rapidly progressive and
devastating):
• intravitreal injections of anti-VEGF
factors: bevacizumab, ranibizumab
• photodynamic therapy (injection of
photosensitizer into systemic circulation
followed immediately by laser targeting
new vessels in macular area)
• combination of above treatments

OPTIC NERVE

 1.2 million cells
 80 % visual fibres
 20 % pupillary fibres
 carries visual
information from
the eye to the brain

OPTIC CHIASM
crossover of nasal fibers
above the pituitary
internal carotids are just
lateral
from optic chiasm:
optic tract to the
lateral geniculate body
opticradiation to the
primary visual cortex

Anterior to Optic
Chiasm
- compressive optic neuropathies
- toxic/nutritional optic neuropathies

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 tumour
compressing any part of the optic nerve
 THYROID EYE DISEASE

Thyroid Eye Disease
 may occur in the absence of biochemical
evidence of thyroid dysfx
 autoimmune reaction (IgG Abs) causing:
 inflammation of EOMs: pleiomorphic cellular
infiltration associated with increased secretion
of GAGs and osmotic imbibition of water
• muscles can become up to 8 times their original
size!!
 no relation to severity of thyroid dysfx!

Thyroid Eye Disease
 main findings: (not all are always present!)
 soft tissue involvement
 lid retraction
 proptosis
 optic neuropathy
 restrictive myopathy

Thyroid Eye Disease
 vision loss from:
 exposure keratopathy
• due to severe proptosis resulting in incomplete lid
closure → chronically exposed cornea → corneal
ulceration & exposure keratopathy
 optic neuropathy
• affects 5% of pts
• compression of ON or its blood supply by
congested (enlarged) EOMs
• can lead to severe, permanent visual impairment
• rx with steroids, surgery if needed

Toxic/Nutritional Optic
Neuropathies
 nutritional deficiencies
 alcohol-tobacco amblyopia

Nutritional Deficiencies
 pts with extremely poor diets, often in association
with alcohol-tobacco amblyopia
 usually due to B12 deficiency in combination with
cyanide toxicity
 symmetrical VF loss
 if early, can be treated with high-dose vitamins
and restoration of « well-balanced diet »
 eventually leads to optic atrophy and permanent
vision loss

Alcohol-Tobacco Amblyopia
 affects heavy drinkers, cigar and pipe smokers: deficient in
protein and the B vitamins
 symptoms: insidious, bilateral, progressive visual
impairment + dyschromatopsia
 signs: symmetrical VF defect, may have pale (or normal)
discs
 rx: 1000 units of hydroxocobalamin qweekly X 10 wks +
multivitamins + « well-balanced diet »
 px:
 good in early cases if comply with rx

 advanced cases: optic atrophy and permanent visual

loss

Optic Chiasm Lesions
- pituitary adenoma

Pituitary Adenoma
 presentation usually in early adult life or
middle age
 symptoms:
 h/a
 visual symptoms: very gradual onset (often
not noticed by pt until very well-established)
• VF defect: usually, bitemporal hemianopia, worst in
the superior field, and extending inferiorly
• colour desaturation across vertical midline
• optic atrophy: in 50% of cases with field defects
caused by pituitary lesions

Pituitary Adenoma
 investigations:
 MRI: coronal, axial and sagittal sections before
and after gadolinium injection
 CT: demonstrates enlargement or erosion of
the sella
 endocrinological investigation: PRL, FSH, TSH,
GH

Pituitary Adenoma
 treatment options:
 observation
 medical: dopamine agonists (bromocriptine)
 surgery
 radiotherapy: often used as an adjunct
 gamma knife stereotactic radiotherapy

visual loss compressed

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