Disorders of the Globe Flashcards
difference between ophthalmologist and optometrist
ophthalmologist - eye surgeon and can treat a wide variety of eye related disorders (MD)
optometrist - treats eye related disorders (OD)
Global traumas include
globe rupture
globe lacerations
intraocular foreign bodies
corneal foreign bodies
Globe rupture is when
full thickness eye injury to sclera/ cornea –> orbital contents spill from the globe
commonly from: penetration/perforation/laceration or rupture due to blunt force trauma
Globe ruptures have a risk for
endophthalmitis - infection of the interior of the eye
hx of trauma
sudden moderate to severe eye pain
+/- decreased vision, obvious FB
Hyphema or associated facial trauma
deviated pupil toward the laceration (tear drop shaped)
severe subconjunctival hemorrhage
Globe rupture presentation
Globe rupture workup
do not apply pressure to the globe
snellen card - visual acuity
assess conjunctiva, looking for defects, visible FB, lacerations
examine pupil for reactivity and shape
slit lamp exam
Globe rupture treatment
do NOT remove FB - immediately refer to ophthalmologist
eye shield NOT a patch
analgesia and antiemetics - avoid vomiting b/c increases IOP
update tetanus
abx prophylaxis
Globe rupture treatment
do NOT remove FB - immediately refer to ophthalmologist
eye shield NOT a patch
analgesia and antiemetics - avoid vomiting b/c increases IOP
update tetanus
abx prophylaxis - prevent endophthalmitis
Intraocular FB can be due to
trauma, sports, occupational injuries
precipitating cause of globe rupture
Intraocular FB workup
slit lamp
+/- fluorescein
CT test of choice, MRI if inconclusive
MRI contraindicated if possibly metallic FB
Intraocular FB treatment
maintain high index of suspicion for globe injury
immediate referral to ophthalmologist
should be removed within 24 hours
increased risk of infection
Lacerations usually associated with
penetrating trauma
Treatment of laceration
minor conjunctival lacerations (<1cm or only partial thickness) - topical abx, patching, close f/u
severe (<1cm) - referral to ophthalmologist, possible suture
corneal FB - most are
superficial and benign
Corneal FB commonly include
metal, wood, plastic
may see ‘rust ring’ if metal
Corneal FB - FB is usually present on
cornea or under upper eyelid
Corneal FB workup
Examination with slit lamp +/- fluorescein
eval for corneal abrasion or rupture
improves visualization of FB
visual acuity - get baseline
Treatment of Corneal FB
visual acuity - baseline
local anesthetic then attempt to remove
try saline flush first
can use needle or cotton applicator if doesn’t come out with flush
bacitracin-polymyxin ophthalmic ointment
tetanus
OTC analgesics
don’t need to patch the eye
Blowout fractures are associated with
periorbital blunt or penetrating trauma (direct - force to bone and indirect - force to globe)
Blowout fractures most commonly affects the
orbital floor (maxilla)
Blowout fractures may result in
entrapment of the orbital tissue and inferior rectus muscle (will have difficult of vertical eye movement)
Palpable step-off at the orbital rim
orbital crepitus
limited vertical eye movement (IR entrapment)
periorbital ecchymosis (black eye)
diplopia (during vertical eye movement)
severe pain
paresthesia and numbness in the infraorbital area
enopthalmos and exophthalmos
blowout fracture presentation
Blowout fracture workup
CT Head and Orbits test of choice
Blowout fracture treatment
all get prophylactic broad spectrum abx
if non-displacement and no globe injury – pain control, ice, decongestants, avoid nose blowing, +/- oral steroids, no operative treatment needed
Indications for surgery in a blowout fracture
severe pain and or autonomic disturbance (entrapment of muscle)
diplopia due to limited eye movement
persistent/severe enopthalmos
fractures involving more than 50% of the orbital floor
goal of surgery in a blowout fracture is
to restore herniated structures into orbital cavity
Corneal abrasion is a
scratched cornea - scratched eye
scratching or scraping away of some of the corneal epithelium
one of the most common ophthalmic injuries
Corneal abrasions are most commonly from
rubbing eyes, FB, contacts, etc
Corneal abrasion presentation
FB sensation
pain and photophobia
difficulty opening eye
blurred vision
redness in the affected eye
excessive lacrimation
Corneal abrasion workup
measure and record visual acuity
slit lamp exam with fluorescein
Corneal abrasion treatment
most will heal on their own in 24 to 48 hrs
try to remove FB if visible
Administration of topical anesthetic (NOT to go home with)
topical broad spectrum abx x 3 days - contact lens wearers need coverage for pseudomonas (cipro)
cold compresses
oral NSAIDs
discontinue lens wear - glasses instead
What can a corneal abrasion lead to
corneal ulcer
Corneal ulcer is a
keratitis = inflammation of the cornea
most common cause of a corneal abrasion
infection (bacterial, viral, fungi, amoeba)
major complication of contact lens wearers, esp overnight
What other causes can lead to a corneal ulcer besides infection
severe dry eye
severe allergic eye disease
inflammatory disorders that involve the eye
Corneal ulcer presentation
eye pain
photophobia
lacrimation
reduced vision
circumcorneal injection
+/- purulent or water discharge
cornea appears hazy, with visible ulcer
hypopyon - layering of WBC in anterior chamber
Corneal Ulcer workup
measure and record visual acuity
slit lamp with fluorescein
ulcer scraping for gram stain and culture
urgent referral to ophthalmologist - risk of permanent corneal scarring and or intraocular infection
Corneal ulcer treatment infectious vs non-infectious
topical abx - levofloxacin, ciprofloxacin (vanco is MRSA is present)
oral or topical antivirals
should heal within days to weeks - heals more slowly in people who smoke
What is the main retinal blood supply
central retinal artery
retinal detachment is when
there is separation of the neurosensory layer from the retinal pigmented epithelium and choroid
most common over the age of 50
What can happen in a retinal tear with vitreous fluid
the vitreous fluid leaks through the retinal tear, behind the retina, pulling it away from the epithelium and choroid
Risk factors to retinal detachments
nearsightedness (myopia)
cataract surgery
diabetic retinopathy
penetrating or blunt ocular trauma
older age
+FHx of retinal detachment
Retinal detachment presentation
painless vision changes
unilateral photopsia (flashers)
increasing number of floaters in affected eye (move in and out of central vision)
decreased visual acuity
metamorphopsia (wavy distortion of an object)
Retinal detachment workup
primarily clinical dx
+/- retinal tear on fundoscopic
if trouble visualizing retina –> ocular US
Retina detachment treatment
emergent referral to ophthalmology
usually surgical intervention - retinopexy
Central Retinal Artery Occlusion (CRAO) aka
ocular stroke
CRAO mean age presentation
early 60s
risk factors of CRAO
similar to other thromboembolic diseases
(Atherosclerosis, hypertension, DM, smoking, hyperlipidemia, hypercoagulable states, male gender, migraine, OCPs)
1/3 of pts with CRAO have ______ carotid artery _____
ipsilateral
stenosis
most common etiology of CRAO
embolism – retinal hypoperfusion, rapidly progressive ischemic damage
visual loss can be partial or total
CRAO presentation
sudden, painless, transient monocular vision loss
lasts 20 - 30 min (never more than 30 min)
described as a ‘curtain coming down’
normal IOP, anterior chamber exam and extraocular movements
Likely carotid bruit
CRAO presentation
sudden, painless, transient monocular vision loss
lasts 20 - 30 min (never more than 30 min)
described as a ‘curtain coming down’
normal IOP, anterior chamber exam and extraocular movements
Likely carotid bruit
cherry red spot on the fovea*
CRAO workup
fundoscopic exam - pallor swelling of the retina, cherry red spot at the fovea, retinal arteries with ‘box-car’ segmentation, +/- clot in the central retinal artery or its branches
if sx onset < 6 hrs - CT head without contrast to r/o intracranial hemorrhage - possible thrombolytics
stroke workup, cardiac assessment, GCA workup if less than 50
CRAO treatment
emergent referral to ophthalmology - irreversible vision loss begins in the first 90-120 min
lysis of clot and restoration of retinal perfusion (vasodilators, meds to reduce IOP, early intra-arterial or intravenous thrombolysis - tPA)
Central Retinal Vein Occlusion (CRVO) main risk
arteriosclerosis
also glaucoma
CRVO is
venous thrombosis –> venous stasis, retinal edema, hemorrhage
retinal ischemia - increased vascular endothelial growth factor - edema and neovascularization - prone to bleeding
endothelial injury
stasis
hypercoag =
virchows triad
CRVO presentation
sudden onset unilateral blurry or distorted vision - decreased visual acuity
fundoscopic exam : dilated and tortuous retinal veins, blood streaked retina or flame shaped hemorrhages radiating from optic disc
cotton wool spots esp w/ hypertension
CRVO treatment
urgent referral to ophthalmologist
no totally effective prevention or tx
management of neovascularization and macular edema - intravitreal injection of anti-VEGF agent, intravitreal steroid injections
optimize risk factors
Macular degeneration affects mostly
the elderly
idiopathic
macular degeneration is a degenerative process that leads to
atrophy of retinal pigment epithelium which causes geographical atrophy and gradual decline of vision
two types of macular degeneration
wet and dry
wet macular degeneration on fundoscopic exam
revealing scarring and hemorrhaging on the retina
dry macular degeneration on fundoscopic exam
deposits of lipids (drusen) beneath the retinal pigment epithelium
size of drusen effects the
amount of vision lost
macular degeneration presentation
painless vision changes
NO redness
usually bilateral
slow, insidious central vision loss
distorted images
macular degeneration treatment
goal to prevent further degeneration
ocuvite - “eye multivitamin”
smoking cessation
lifestyle modifications
laser photocoagulation
anti-VEGF agents
Diabetic retinopathy two types
non-proliferative (just hemorrhage or exudate, no abnormal blood vessels) and proliferative (abnormal blood vessels on fundoscopic exam plus others)
Diabetic retinopathy treatment
annual dilated eye exam for all at risk patients
risk factor modifications
without sx - monitor closely without treatment
with sx - intravitreal injections of an anti-VEGF
Iritis is
inflammation of anterior or posterior chamber and iris - not a true ocular emergency
most cases of iritis is from
idiopathic
blunt for trauma - 20%
other immune, traumatic or infectious mechanisms
acute iritis presentation
pain
redness
photophobia
tearing
decreased vision
with pain developing over a few hours or days
chronic iritis presentation
blurred vision
mild redness
with little pain or photophobia except during an acute episode
Iritis treatment
aimed at reducing inflammation and pain/ preventing complications
atropine - 1st line topical cycloplegic (paralyze the ciliary bodies)
refer to ophthalmologist within 24-48 hours
