vision abnormalities Flashcards
what is presbyopia
aging eyes
normal aging in middle age– usually by 45 or so
what does presbyopia cause
refractive error for close vision (can’t see up close)
eye strain
headaches
what happens to the lens in presbyopia
lens gets harder and less flexible with age and stops focusing light correctly onto the retina
how to treat presbyopia
corrective lenses
how to assess presbyopia
eye exam
three types of glaucoma
acute angle closure
chronic angle closure
chronic open angle
what is glaucoma
damage to the optic nerve from pressure inside the eye
Glaucoma risk factors
individuals with first degree relative
DM
affected ethnic groups (shape of eye)
pts using long term steroid therapy
form of glaucoma caused by rapid narrowing or closure of the anterior chamber angle
(sudden, matter of seconds)
acute angle closure glaucoma
inadequate drainage of the aqueous humor leads to increased IOP and damage to the optic nerve
acute angle closure glaucoma
acute angle closure glaucoma risk factors
shallow anterior chamber which is associated with far sightedness or small eyes
genetics/ancestry
elderly
extreme pain and blurred vision (sudden although can be subacute headaches)
unilateral
halos around lights
headaches
nausea/ abdominal pain
red eye/cloudy cornea/dilated pupil
eye feels hard on palpation
acute angle closure glaucoma patient presentation
acute angle closure glaucoma precipitated by
pupil dilation
(they went into dark room, pupils dilated, then vision loss)
acute angle closure glaucoma pressure
well over 50
(normal IOP 10-21)
acute angle closure glaucoma treatment
emergent referral to ophthalmology
reduce IOP:
- IV acetazolamide
- followed by oral acetazolamide
- plus topical medication (timolol maleate)
- topical pilocarpine (after IOP starts to fall)
cataract removal or laser peripheral iridotomy to follow
chronic glaucoma symptoms
may be no symptoms (or not noticed) until disease has progressed for a long time
progressive optic nerve damage
leads to visual field loss and ultimately, irreversible blindness if left untreated
gradual loss of peripheral vision “tunnel vision”
chronic glaucoma
chronic glaucoma often suspected on
routine eye test
optic nerve cupping: looks like a pale cup
nerves don’t connect
chronic glaucoma vision loss
chronic glaucoma prevention
screen patients with IOP measurements and optic disk exam if
inuit or asian ancestry
affected 1st degree relative
DM
older people with African or hispanic ancestry
long term oral, intranasal, and inhaled corticosteroid use
increased aqueous production and/or decreased outflow are possible mechanisms for elevated IOP
most common and usually bilateral
open angle chronic glaucoma
chronic low vascular perfusion, Raynaud’s phenomenon, migraine, nocturnal systemic hypotension and over treated systemic hypertension
normal tension chronic glaucoma
flow of aqueous humor is obstructed
similar to acute form, can have eye redness, discomfort, and headache
progression much slower
may have only mildly elevated IOP
angle closure chronic glaucoma
the outer rim tends to be orange or pink in color and contains the nerve fibers
disc
(in the center) is a pit where there are no nerve fibers – this is where blood vessels enter the eye
cup
the disc takes on a hollowed out appearance on fundoscopic exam from the death of smaller nerves around the optic nerve
cupping
the cup should not make up more than _______ of the total area of the optic nerve
30%
what happens to central vision in glaucoma
remains good until late in disease
glaucoma diagnosis
consistent and reproducible abnormalities in at least 2 of 3 parameters:
optic disk
visual fields
intraocular pressure
chronic glaucoma treatment
- prostaglandin analog drops: reduce IOP (latanoprost, travoprost, latanoprostene bound)
- topical beta blockers: reduce production of fluid
- laser treatment or surgery if medication fails: open up space to improve flow of aqueous humor
(trabeculoplasty, trabeculectomy, iridectomy)
what causes strabismus
problems with the eye muscles
nerves that transmit information to the muscles
control center in brain that directs eye movements
misalignment of the eyes
strabismus
strabismus usually presents in
children
eye deviated inward
esotropia (strabismus)
eye deviated outward
exotropia (strabismus)
epicanthal skin folds cover the medial canthus
lack of development of the bridge of the nose
pseudostrabismus
what tests do you do for strabismus
Hirschberg test to see if white light is in same spot on pupil
cover test to see if bad eye will move into place
risk factors for amblyopia
prematurity
small size for gestational age
first degree relative with amblyopia
neurodevelopmental delay
functional reduction in visual acuity caused by abnormal visual development early in life
most common cause of pediatric visual impairment
unilateral
often associated with impaired or absent fine depth perception
amblyopia
abnormal binocular interaction and long term suppression of one eye
strabismic amblyopia
appropriately focused visual stimuli are crucial to the development of
normal vision
critical period of visual cortex neuroplasticity
affected children are often diagnosed at the first vision screening when they are old enough to identify letters or figures (typically 4-5 years)
refractive amblyopia
visual acuity typically reaches the adult level by
3-5 years of age
growth on eyelid
deprivational amblyopia
amblyopia diagnosis
complete eye exam by skilled eye care specialist
defined as >2 line difference in visual acuity between eyes
what does amblyopia screening include
vision risk assessment at all health maintenance visits and vision screening at 3,4, and 5
objection to occlusion test
(amblyopia: preverbal screening and referral)
monitoring Childs response to alternate occlusion of the eyes
who should be screened for amblyopia
all children younger than five
during objection to occlusion test what can you expect from children with moderate to severe visual impairment in one eye when the eye with better vision is occluded
become irritable
children with suspected amblyopia should be referred to a
pediatric ophthalmologist or optometrist
indications for amblyopia referral
- visual acuity worse than 20/40 in a child 3-5 or worse than 20/30 in a child 6 or older
- visual acuity difference > 2 lines between eyes
- strabismus
-abnormal red reflex - asymmetry of vision
- unilateral ptosis or other lesions that threaten the visual axis
amblyopia treatment
occlusion therapy (patching better eye)
atropine
fix structural problems
retinal tumor of childhood
67% diagnosed before the age of 2, rare after 6
retinoblastoma
most common presenting symptoms of retinoblastoma
leukocoria (white reflex) or strabismus
retinoblastoma diagnosis
fundoscopic exam under anesthesia with maximally dilated pupil
imaging studies to confirm and evaluation for extension
retinoblastoma management
ophthalmology and oncology
transient emboli to a retinol artery
carotid artery stenosis
amaurosis fugax
this is a symptom
sudden unilateral vision loss
painless
typically lasts a few minutes
like a curtain going down and then up
amaurosis fugax
how do patients present with amaurosis fugax
almost always present after transient visual loss episode has resolved
- neurologic and ophthalmologic exam is usually normal
Amaurosis fugax: differential diagnosis
carotid artery disease
giant cell arteritis
(swelling of the arteries of the head reduces blood supply)
(usually with pain and headache)
amaurosis fugax: evaluation
> 45
ischemic cause likely
amaurosis fugax: evaluation
< 40
benign migrainous cause likely
Amaurosis fugax: exam
visual acuity
visual fields
examination of optic fundus
carotid artery
Amaurosis fugax: evaluation
- ophthalmologic evaluation
- erythrocyte sedimentation rate and C-reactive protein
- carotid imaging
what to do if initial testing for amaurosis fugax is normal
Cardiac evaluation
brain MRI
EEG
hypercoagulable testing
Amaurosis fugax treatment
depends on the cause
treat like stroke until proven otherwise
