Transcript Acute Vision Loss Introduction

Acute Vision Loss
Dan Mayer, MD
Professor of Emergency Medicine
Albany Medical College
Introduction - True emergencies
• Immediate ophthalmologic evaluation:
1. Central retinal artery occlusion
2. Retinal detachment
• Next day ophthalmologic evaluation:
1.
2.
3.
4.
Central retinal vein occlusion
Branch artery occlusion
Vitreous hemorrhage
Maculopathies
• Other causes (toxins and trauma)
Anatomy of Vision - Normal visual
axis/anatomy of the eye
Anatomy of Vision - Normal visual
axis/anatomy of the eye
Anatomy of Vision - Anatomic
Classification
1. Brain
2. Optic nerve
3. Blood vessels
a) Ophthalmic artery
b) Choriocapillaris
c) Central retinal artery
d) Cileoretinal artery
4. Macula/Retina
a)
Macula-photopic
vision
b)
Peripheral fields
scotopic vision
c) Anterior
chamber
5. Lens
Examination for Vision Loss
1. Visual acuity
2. Pupillary reaction
a) Marcus-Gunn Pupil
b) Irregular pupil
3. Anterior chamber
a) Ophthalmoscope
b) Slit lamp
Examination for Vision Loss
4. Fundus – indirect and direct
ophthalmoscopy
a) Direct examination as a
screening tool
b) Indirect examination to
better see peripheral retina
5. Extra ocular motion
6. Cornea
Central Retinal Artery Occlusion
1. Total painless
monocular vision
loss
a) May be preceded
by brief transient
episodes
b) Caused by micro
emboli
Causes of Central Retinal Artery Occlusion
a)
b)
c)
d)
e)
f)
g)
Atherosclerotic plaque in the carotid
Embolus from a cardiac valve
Systemic vascular disease
Hyperviscosity syndromes
Trauma – fat emboli
Oral contraceptives
Systemic diseases – DM, syphilis, sickle cell
disease
h) Injections of medications around the head and neck
i) Temporal arteritis
j) Drug abuse
Examination for CRAO
1.
2.
3.
4.
5.
Visual acuity – finger
counting, light perception,
or nothing
Pupillary reaction –
consensual but not direct\
Fundus – pale with dark
veins and narrow arteries
Fovea intact – cherry red
spot
‘Box car’ appearance of
retinal arteries
Treatment of CRAO
Relief of vasospasm – increase pC02 by:
i. Paper bag rebreathing
ii. Breathe a mixture of 95% 02 and 5% C02
5. Attempt to dislodge clot – direct occular massage
6. Acetazolamide or mannitol IV. Aspirin and
acetazolamide continued for two weeks
7. Immediate ophthalmologic consultation for anterior
chamber paracenteses
i. Anesthetize lens
ii. 27G needle – corneal limbus at 4 & 7 o’clock
iii. Allow 2 - 3 drops of aqueous to escape
4.
Outcomes of CRAO
1. Low success rate - 35% achieve any useful vision
2. Check sed rate – (if over 50 in person over 50) =
steroids
3. Branch artery occlusion
4. Amaurosis fugax
a)
b)
c)
d)
e)
f)
“flight blindness”
“curtain coming down”
Transient unilateral vision loss
Platelet-fibrin emboli from ulcerated/stenotic carotid
“Hollenhorst plaques”
Examination
i. May be normal
ii. Check for carotid bruits, cardiac murmers, or dysrhythmias
g) Treatment
i. Follow up with neurologist or internist
ii. Interval treatment with aspirin and dipyridamole
Retinal Detachment - Pathophysiology
1. Separation of the
outer retinal pigment
epithelium from the
inner sensory layer
2. Fluid accumulation
between the layers
causes the separation
Retinal Detachment - classification
1.
2.
3.
Rhegmatogenous – most common; caused by breaks in the
retina
i. Liquid into the hole with enough force to separate the
layers of the retina
ii. Hole caused by vitreous collapse
iii. Also caused by degeneration of the retina
iv. Other intrinsic defects
Traction – pulling force on the retina creates a subretinal space
without a tear
i. From fibrous vitreo-retinal bands
ii. From diabetic neuropathy or old trauma
Exudative – chorioretinal vessel leak
Causes of Retinal Detachment
a)
b)
c)
d)
More common in men
Average age 56 years
Bilateral in up to one third
Associates with:
a)
b)
c)
d)
Degenerative myopia – related
to degree of myopia
Aging with lattice degeneration
of the vitreous
Aphakia – post cataract surgery
Absence of the lens (aphelia),
diabetes, sickle cell disease,
toxemia of pregnancy, severe
kidney disease, trauma with up
to 40 year latency after the
trauma
Rate is 10 per 100,000
people per year
Gradual or total loss of vision
1. Cloudy or smoky vision –
shadow or curtain
2. Flashes of light-photopsia,
or floaters
3. Visual acuity normal until
macula is involved
Examination
a) Fundoscopic examination
with indirect
ophthalmoscope
b) Grey retina with folds and
abnormal choroidal pattern
c) Holes, tears or undulating
appearance of the retinal
vessels
Always check other eye
Clinical Features of
Retinal Detachment
Treatment of Retinal Detachment
Surgical treatment in rhegmatogenous detachment:
i.
ii.
iii.
iv.
Seal holes with lasers or cryotherapy cautery
Scleral buckle or banding
External drainage of subretinal fluid
Bed rest with elevation of the head
Visual recovery is time dependent
i.
ii.
iii.
iv.
v.
Depends on whether and for how long the macula is
involved
If pre-op 20/50 or better, 90% same or better
If macular sparing, 80% got 20/50 or better
Macular involvement causes rapidly decreasing vision at
first then slower loss
Only 2% of macular involved cases got back to 20/20
Pathophysiology of Central Retinal Vein Occlusion
1.
2.
3.
4.
Vision loss more gradual than that seen with Retinal Artery
Occlusion
Degenerative disease of the venous endothelium
External compression
Venous stasis
Ischemic vs. nonischemic types
Non-ischemic
has benign
clinical
course
Ischemic –
50% go on
Causes of CRVO
1.
2.
3.
4.
5.
Atherosclerotic vascular disease
Arterial hypertension
Diabetes
Hyper viscosity
Open angle glaucoma, trauma,
closed angle glaucoma, vascular
hypertension
6. Painless monocular visual loss
a. Branch occlusion-partial vision loss
b. Preceded by transient decrease in vision
c. Blurred vision getting better throughout
the day
Differential diagnosis CRVO
1.
2.
3.
4.
5.
6.
7.
8.
Diabetes
Blood dyscrasias
Congenital tortuosity
AVM and retinal
vascular angiomas
Papilledema
Pseudotumor cerebrii
Congenital heart
disease
Shaken baby syndrome
Examination of CRVO
Visual acuity – near normal or
markedly decreased
Visual fields – central or
peripheral field cut
Funduscopic examination:
i. Engorged venules
ii. Retinal hemorrhages
iii. Retinal edema
iv. “Blood and thunder”
fundus – large and
small hemorrhages and
cotton wool patches
Treatment of CRVO
Treat underlying disease
No proven treatment but
spontaneous resolution
common
Laser photocoagulation to
prevent
neovascularization
Ischemic CRVO
Pathophysiology Vitreous Hemorrhage
May start in retinal vessels,
choroid or ciliary body
Visual loss depends on the
amount of bleeding
i. Minor – “floaters”
ii. Moderate – black
streaks/black dots
iii. Major – profound
painless visual loss
Blood clots rapidly and sinks
in 1-3 days
Causes of Vitreous Hemorrhage
Proliferative retinopathy
i.
ii.
Diabetic – 34-40%
Sicle cell – 1%
Retinal tear – 12-22%
Rhegmatogenous retinal
detachments – 6-15%
Vein occlusion – 10-13%
Posterior vitreous detachment –
Up to 12%\
Intraocular lens – Up to 3%
Miscellaneous – Up to 7%
i.
ii.
Trauma
Hypertension
Retinal detachment – Up to 10%
Idiopathic – Up to 7%
Examination Vitreous Hemorrhage
a)
b)
c)
d)
e)
f)
g)
Anterior chamber cells and
flare
Rubeosis iridis – vessels on
anterior iris
Red reflex absent or decreased
Retinal details not seen
Color of hemorrhage from red
to black to white
Hemorrhage may appear as
dispersed blood, sheets, or
focalized ‘clots’
Ultrasonography to detect if
retinal tear is present
Treatment of Vitreous Hemorrhage
1. Bed rest with elevation of
the head
2. Photocoagulation
3. Surgery
4. Clears in days to weeks
depends on size and
recurrence
5. Complications –
glaucoma and connective
tissue proliferation
Pathophysiology Maculopathy
1.
2.
Destruction of the macula
Causes
a)
Inflammatory
i. Bacterial
ii. Viral
iii. Portozoan
iv. Autoimmune
b) Degenerative
i.
ii.
iii.
iv.
Primary – genetically determined
Secondary – trauma, radiation,
vascular disease, inflammation and
other degenerative disorders
Macular degeneration of aging –
most common cause of blindness in
elderly
Retinal Drusen
Maculopathy
c) Hemorrhagic – Retinal Hemorrhage
i. Trauma, vascular, obstruction,
vasculitides, neovascularization,
degeneration of the retina, and high
myopia
ii. Systemic causes – Diabetes,
hypertension or blood dyscrasias
d) Visual loss depends how much
macula is involved
i. Involvement away from the macula –
floaters
ii. Pain or heaviness of the eye with
anterior chamber involvement
iii.May present with gradual loss of vision;
metamorphopsia – straight lines appear
curved; micropsia – objects appear
smaller than they are
iv.Sudden painless loss of vision if
hemorrhage
Diabetic retinopathy
Examination Maculopathy
Fundoscopic examination depends on etiology
of inflammation
i.
ii.
Exudation and inflammatory cells in the
vitreous
Inflammation destroys the retinal pigment
epithelium the choroid appears bright red
Visual acuity is best test for macular
involvement
Hemorrhagic type of maculopathy, shape=site
SITE
Superficial retina
Superficial nerve fiber layer
Substance of retina
Layer between retina and choroid
Pigment layer
DESCRIPTION
Large meniscus
Linear
Punctate
Large and red
Large and dark
Maculopathy
4.
5.
Lab – Skin testing for
histo and tbc, CF testing,
viral titres including HIV,
and HLA typing
Treatment
a)
b)
c)
Inflammatory – treat
underlying inflammation
Photocoagulation in some
cases of hemorrhage
Treatment directed to the
underlying disease
1.
Neurogenic toxicity to the ganglion cells of the retina,
optic nerve fibers, or secondary vascular disturbance
Causes
2.
a)
b)
400 medications which have toxic effects on vision
Accidental or intentional
i.
ii.
iii.
iv.
c)
Methanol
Quinine
Ergot derivatives
Salicylate
Complications of therapy
i.
ii.
iii.
iv.
v.
vi.
vii.
Cisplatinum
Combined endocrine agents
Combined antihypertensives
Deferoxamine
Ergot derivatives
Hexamethonium
Parenteral steroids
Toxins
Methanol
Toxic metabilites – formate act on the optic nerve
General symptoms – Mausea, vomiting, abdominal
pain, headache, dizziness, delerium, stupor and coma
Visual disturbances ‘like a snowstorm’
1)
2)
a.
b.
c.
d.
Sudden with permanent complete blindness
Impaired pupillary light reflex and accomodation
24 hours for fundoscopic examination to become abnormal –
then get hyperemia of the disk, retinal edema and engorgement
of retinal vessels
Management
i.
ii.
iii.
Ethanol level to 100mg%
Dialysis
Bicarbonate therapy
Cinchona alkaloid
a.
Cinchonism – flushed diaphoretic skin, visual disturbances, tinnitus,
headache, confusion, delerium. Coma, seizures, nausea, vomiting,
diarrhea, hypotension, and cardiac conduction abnormalities
i.
ii.
iii.
b.
Quinine
42% had visual disturbances
Sudden loss or deterioration of vision bilaterally
Constricted visual fields, scotomata, night blindness, decreased color
perception, and photophobia
Dilated unreactive pupils, with normal or pale optic nerve atrophy
i.
ii.
iii.
Mild poisoning – reversible
Severe poisoning – some residual
Permanent blindness if there is vasospasm
Ergot Derivatives
1)
Poisoning – ingestion of large amounts
of produce abortion
a.
b.
2)
Reduced vision and constriction of
peripheral field
a.
b.
3)
Alpha adrenergic blocker and direct
stimulation of peripheral and cranial blood
vessel smooth muscles
Headache, vomiting, diarrhea, dizziness,
hypotension, hypertension, drowsiness,
convulsions, and coma
Pupils are dilated and poorly reactive to
light
Fundi Normal, or slight edema with
narrowing of the retinal arteries
Treatment is with usual poisoning
treatment and vasodialtors. Loss is
usually reversible
1) Vision loss and tinnitus
a.
Direct toxicity to the
ganglion
b. Decreased vision,
headache, tinnitus,
dizziness, decreased
hearing, confusion
c. Nystagmus, dilated pupil
which is reactive, and with
constricted visual field
d. Fundus is normal or with
constricted arteries
2) Treatment – alkalinization
of the urine, and dialysis
in severe overdose –
recovery is the rule
Salicylates
1) MS most common cause – 13 to 36 %
a. 27 – 37 % of MS patients will get it
b. Retrobulbar pain
2) Other causes
Optic Neuritis
a. Tobacco-alcohol amblyopia (nutritional cause)
b. Vision loss with central scotoma and retrobulbar pain
c. Collagen vascular disease or parachiasmal meningioma
3) Examination
a. Marcus-Gunn Pupil
b. Fundus is usually normal
i. When optic nerve involved – blurred, hyperemic, elevated,
and may look like papilledema
ii. Usually unilateral, more decreased vision than in
papilledema
c. CBC, Sed rate, Glucose, CT of the head, LP, MRI (test
of choice for MS)
4) Treatment
a. Gradual partial improvement
b. Steroids and ACTH may speed resolution
Migraines
1) Retinal migraines cause spasm of the retinal
artery
2) Examination – will be normal or show some
pale retina with macular sparing
3) Treatment – standard treatment for migraines
(Thorazine/Thorazine-DHE/MetoclopramideNaproxyn)
Temporal Arteritis
1) Muscle aches and pains, recurrent
headache, and jaw claudication, and
systemic symptoms such as fever,
weight loss and anemia
2) Marcus Gunn pupil and engorged
disk with dilated capillaries
a. Tenderness over the temporal artery may
not be present
b. Suspect in any patient over 50 years of
age
c. Lab workup includes CBC, Glucose, Sed
rate, VDRL, fibrinogen, and lipid survey
3) Treat empirically if any suspicion
and elevated sed rate
a. Use of steroids can result in sparing of
vision
b. Use 60mg of prednisone
c. Treat before results of biopsy are
available
Hyphema and other trauma
1)
Retinal detachment & vitreous
hemorrhage
2)
Commotio retinae (edema)
3)
Complications – pain, photophobia,
acute and chronic glaucoma, blood
staining of the cornea, vitreous bleed,
hemophthalmitis, inflammatory reaction
4)
Grading of hyphemas
a. I – 1/3 of anterior chamber is filled
b. II – 1/3-1/2 filled
c. III- over ½ filled
Edwards 1973 – 184 patients with unilateral
hyphema
i.
Age: 1-61 with mean age of 12 years
ii. Complications: 35% - rebleed, 52%
return of 20/50 or better vision.
Complication rate higher if rebled
iii. Rebleed rate and return of vision
depends on grade
Spontaneous bleed
Grade
I
II
III
% Rebleed
23
35
65
% Return
≥ 20/50
80
70
30
Examination of Eye Trauma
Slit lamp examination – anterior
chamber blood
CT scan or ultrasound of the globe
Periodic reevaluations as the blood
clears to check for retinal tears
Treatment – Gorn 1979
a.
b.
c.
d.
Aspirin increases the rate of
bleeding
Put the eye at rest with sedation
and elevation of the head
Dilatation decreases the rate of
rebleeding
Small hyphemas with very
reliable patients, home rest with
patching and close follow up
Complications of Trauma
Rebleeding with the
formation of secondary
glaucoma or pigment
staining of the cornea
with visual loss
Delayed retinal detachment –
80% seen within two
years of the trauma and
usually with ora serrata
tears. Require surgical
treatment – scleral
banding
Hysteria
1)Functional rather than organic disorder
2)Subconscious expression of nonorganic signs or
symptoms
3)Usually very little insight is present
4)Examination
a.Normal pupillary reaction and fundus
b.Red/green glasses test
c.Opticokinetic nystagmus response
d.Magic drop test
QUESTIONS?