20/200 vision after correction in the better eye
or
Binocular visual field subtending 20 degrees or less.
What are the IRS requirements to be legally blind?
Corneal Abrasion
-Damage to the corneal epithelium.
-Often caused by fingernail, sand, contact lens.
-Slow healing in smokers.
S/S:
Severe pain, photophobia
FB sensation, Tearing, Red eye.
Diagnostic:
Fluorescein dye with any cobalt-blue light.
Appears as yellow fluorescence of the basement membrane
Treatment:
Drop of topical ophthalmic anesthetic (only once!)
Remove Foreign body with moistened cotton-tipped
Antibiotics for large abrasions/contact lens wearers.
Bacitracin-polymyxin ointment
Fluoroquinolone topical for contact wearers.
Patching (not recommended)
Mydriatic/topical NSAIDs for pain.
Infectious Keratitis
Pathophysiology: Infection of the cornea
Foggy looking, can find a white spot where infection is located.
Causes: Contact lens (esp. overnight), trauma.
S/S:
Red eye and pain (more significant than corneal abrasion)
Excess tears, Eye discharge,
Difficulty opening the eyelid because of pain or irritation.
Blurred vision, photophobia, FB sensation.
Diagnostic:
Slit lamp
Gram stain culture
Treatment:
Topical fluoroquinolones (floxacin) are first-line agents if the prevalence of resistant organisms is low.
Refer emergently to an ophthalmologist.
Herpes
What is a dendritic lesion on the eye indicative of?
Hyphema
Pathophysiology: Blood collection in the anterior chamber.
S/S:
Eye pain, photophobia
Sometimes blurred vision is secondary to obstructing blood cells.
N/V may signal a rise in intraocular pressure (glaucoma) caused by blood cells.
Diagnostic:
Clinical exam
Determine underlying causes (blunt trauma most common)(can be spontaneous)
Management:
Increased risk for vitreous hemorrhage
Prevention of further hemorrhage is the foremost treatment goal.
Keep pt at rest in a supine position with head slightly elevated.
Emergent referral
Avoid any medications with antiplatelet activity (NSAIDS)
Vitreous Hemorrhage
Pathophys: Any blood in the vitreous cavity is known as vitreous hemorrhage (VH)
S/S:
Sudden visual loss
Abrupt onset of floaters that may progressively get worse.
occasionally can see bleeding within the eye.
initial diagnostic:
CIues:
Inability to see fundus details
Presence fo blood in the vitreous in front of the retina.
Initial Management:
Examination by an ophthalmologist is essential.
Intraocular Foreign body
-Foreign body lodges in any part of the eye.
S/S:
Hx of “something in my eye”
Particularly concerning if equipment based propulsion (chainsaw, hammering)
Visual loss or media opacity.
Diagnostic:
X-ray
CT scan
NO MRI!!!!!!!!!!!!!!!!!!!!!!!!
Management:
Emergency treatment by ophthalmologist.
Risk for intraocular infection.
Blow out Fracture
-Fracture of the inferior wall (maxillary sinus) and medial wall (ethmoid sinus through the lamina papyracea)
S/S:
Diplopia (upward gaze)
Entrapment of inferior rectus
Limitation of upward gaze
Tenderness or step-offs at the infraorbital rim.
absent pupillary light reflex → damage to afferent or efferent nervous system.
Edema and periorbital ecchymosis.
Diagnostic:
CT scan
Management:
Refer out.
Globe Rupture
-A break or tear in the eyeball's outer layer (sclera or cornea), leading to intraocular leakage.
-Pathophysiology:
Penetration/perforation/laceration
Rupture due to blunt force.
-Epidemiology:
Children: Sharp objects at home (scissors)
Adults: Workplace injuries, assaults, MVAs.
Elderly: Ground-level Falls.
-S/S:
May be immediate or develop over days/weeks.
Ecchymosis of eyelids
Teardrop pupil
subconjunctival hemorrhage
hyphema
everything
-Diagnostics:
Slit Lamp
Fluorescein staining → stream of clear aqueous fluid originating from the wound site. (Seidel sign)
CT scan
NO pressure on the globe during Evaluation!!!!
ABCs come first.
Ophthalmic exam diagnosis
Treatment:
Patient is NPO
Urgent ophthalmology consult
Once the surgery is safe, surgery.
Nystagmus
-A rhythmic, involuntary oscillation of the eyes, typically characterized by repetitive uncontrolled movements.
The most common cause is from drugs (phenytoin), excessive alcohol, or any sedating med.
Congenital: Albinism, Leber’s congenital amaurosis, Bilateral cataract.
S/S:
Repetitive eye movements
Reduced visual acuity
abnormal head postures to minimize the effect
Oscillopsia (illusionary movement of the environment)
Diagnosis:
Eye Examination
MRI or CT may be indicated
Treatment:
Treat underlying cause
Non-urgent referral
Corrective lens
Gabapentin, Baclofen
Surgical interventions
Vision rehab.
Conjunctivitis
-Most common cause of red, irritated eye.
-Self-limited typically, will last 10-14 days if not treated.
Epidemiology:
Viral: Adenovirus
Bacterial: all the common ones
Allergic
Chemical
S/S:
Symptoms:
Discharge
FB sensation, photophobia
Eyelid matting
Signs:
Red eye, mild or no change in visual acuity
Involvement of the bulbar and tarsal conjunctiva.
Diagnosis:
Hx and smear culture.
Treatment:
Empiric treatment for 5-7 days:
Polymyxin-bacitracin
Trimethoprim-polymyxin
Ofloxacin (preferred for contact lens)
Erythromycin ointment
Scleritis
-Painful, destructive, and potentially blinding. The pain is constant and boring (very intense) and may radiate to the face and periorbital region.
S/S:
Tearing, photophobia
Globe tenderness to palpation
Painful ocular movement
Red eye
Signs:
The conjunctival vessels are injected.
Initial Diagnostic:
Check intraocular pressure.
Approach to management:
An ophthalmology consult is required.
Treatment varies to underlying disease:
NSAID therapy
Glucocorticoids
Immunosuppressant medications.
Subconjunctival Hemorrhage
-Results from rupture of small vessels bridging the potential space between the episcleral and the conjunctiva.
Usually spontaneous but can result from blunt trauma, eye rubbing, or vigorous coughing.
S/S:
A spectacular red eye
Vision is not affected and the patient often doesn’t realize.
Treatment:
None needed.
Acute Angle-Closure Glaucoma
-Pupil becomes mid-dilated, and peripheral iris blocks aqueous outflow via the anterior chamber angle and the intraocular pressure rises abruptly.
Epidemology/Risk Factors:
Asian Highest risk, far sighted, elderly.
S/S:
Pain, red eye, obscurations, blurred vision, N/V/Headache
Hard eye on palpation
Corneal edema, cloudy cornea
Injections, Pupil moderalty dialated.
Diagnostic:
Measurement of intraocular pressure during acute attack OR
Gonioscope (observing the narrow chamber angle with a mirrored contact lens.
Treatment: (untreated → 2-5 days before vison lost)
Emergent referral.
Acetazolamide (PO or IV)
500mg IV initially
250mg orally QID
Topical betablockers
Prostaglandin analogues
A2-adenergic agonists
Pilocarpine to induce miosis.
Laser Iridectomy
Orbital Cellulitis
-Infection around the orbit (H. Flu, S. Aureus, S. pneumoniae) usually stemming from a sinus or dental infection.
Without treatment → Optic nerve can be damaged by inflammation and infx can spread to cavernous sinus.
Epidemiology:
Pediatric: Ethmoid sinus infection (43-100%)
Adult: Frontal Sinusitis (50%)
S/S:
Recurrent dental or sinus infections
Fever, Proptosis
Restricted ocular movement
Swelling and redness of the eye.
Diagnosis:
Blood cultures
CT of orbits with contrast
Treatment:
Emergent referral to ophthalmology
Immediate treatment with IV antibiotics
Penicillinase-resistant penicillin (nafcillin) AND
Metronidazole or clindamycin
Trauma → Use cephalosporin for S. Aureus/Group A strep. coverage.
Surgery for drainage of abscess.
Blepharitis
-Chronic inflammation of the eyelids that are usually colonized by Staph.
S/S:
Greasy eyelids
Ulcerated Lids
Bumps on the under eyelid.
Crusted with scaling debris that cling to lashes.
Management:
Eyelid hygiene
Warm compresses
Eyelash scrubs with baby shampoo.
Hordeolum
-Caused by Staph infx of the superficial accessory glands of Zei’s or Moll located in the eyelid margins.
Also called a stye.
More common in adults than children.
“shows up overnight”
Can visualize “head”, typically pointed outward.
S/S:
Upper or lower lid
Localized, red, swollen
Acutely tender lesion
Diagnosis → clinical exam
Treatment:
Topical antibiotics (Bacitracin/Polymyxin B Opthalmic ointment.)
Warm compress
Not improving over 48 Hours → incision indicated.
Tx any generalized cellulitis of the lid.
Chalazion
-Granulomatous inflammation of a meibomian gland
This may FOLLOW an internal hordeolum.
High recurrence rate
More common in third decade of life.
S/S:
Painless swelling of the eyelid over weeks or months.
Slowly enlarging and non-tender
Treatment:
Warm compress
Typically completed by ophthalmologist
I&D if not improving in 2-3 weeks.
Corticosteroid injection.
Amaurosis Fugax
-Transient ischemic attack of the retina → interruption of blood flow to the retina for more than a few seconds, resulting in transient monocular blindness.
Typically the result of an embolus in an arteriole
often from atherosclerotic plaque in the carotid artery or aorta.
Risks: (vascular disease)
Giant cell arthritis
Carotid Stenosis
CAD, A-Fib, Valvular disease
Diabetes, Advanced age
S/S:
Sudden-onset monocular loss of vision
Usually lasting a few minutes with complete recovery
Rapid fading vision like a curtain descending, sometimes only affecting a portion of the visual field.
RECOVERY IS KEY!!!!
Diagnostics;
Urgent neuroimaging to asses for cerebral infraction/identify the source of emboli
Ophthalmoscopy shows zones of whitening, edematous retina following the distribution of branch retinal arterioles.
Treatment:
Due to increased risk of stroke, TIA, and MI; treat underlying cause.
Immediate treatment with oral aspirin (81mg or higher)
Central & Branch Retinal VEIN Occlusion
-Blockage in certain vessels in the retina (you have to guess based on the following 🙂
S/S:
Sudden monocular loss of vision
no pain or redness
Widespread retinal hemorrhages
Retinal venous dilation and tortuosity
Retinal cotton-wool spots
Optic disc swelling
Initial Diagnostic:
Screen for diabetes, hyperlipidemia, and hypertriglyceridemia for all patients.
ESR
Antiphospholipid antibodies.
Retinal findings distinguish from arterial occlusion.
Management:
Urgent referral
Intravitreal injection of VEGF (vascular endothelial growth factor)
Central & Branch Retinal ARTERY Occlusion
-Decreased arterial blood flow to the retina resulting in ischemic damage.
S/S:
Sudden monocular loss of vision
no pain or redness
Widespread or sectoral pale retinal swelling.
Diagnostic:
Screen for diabetes, hyperlipidemia, and hypertriglyceridemia for all patients.
ESR and CRP are typically evaluated.
Urgent brain MRI
Obtain duplex ultrasonography of carotid arteries, ECG, and echocardiogram
Ophthalmoscopy: Reveals pale swelling of the retina with cherry-red spot at the fovea.
Treatment:
Emergent referral to ED for stroke evaluation/urgent ophthalmologist referral.
Lay patient flat
Ocular massage
High concentrations of inhaled oxygen
Intravenous acetazolamide
Anterior chamber paracentesis.
Macular Degeneration
-Gradual, Painless, and Bilateral central vision loss
Exudative:
Choroidal layer has new vessel growth under the retina that leads to exudative fluid, hemorrhage, and fibrosis.
Dry:
Accumulation of extracellular deposits called drusen underneath the retinal pigment epithelium.
S/S:
Bilateral central vision loss
no pain or redness
Distortion or abnormal size of images
Wet (10%) → more rapid onset
Dry (90%) → Progressive visual lost due to atrophy or outer retina.
Diagnosis:
Eye Exam with urgent referral to ophthalmologist.
Treatment:
Must be seen and regularly treated by an eye doctor.
No dietary change has been directly linked to prevent development.
Improvement with Vit. C, E, zinc, copper, and carotenoids.
Wet MD → inhibitors of VEGF (ranibizumab)
Drusen
-The Hallmark of Macular Degeneration.
-Extracellular deposits of lipids, proteins, and cellular debris which are found within the layers of the retina and appear as small, yellow deposits on dilated eye exams.
Diabetic Retinopathy
-Complication to diabetes → retina is damaged.
-Chronic high blood sugar → microvascular changes → weakened vessel walls → → vision impairment or loss.
Epidemiology:
33% of all diagnosed diabetic patients.
More common in type 1
S/S:
Reduction of vision
Diagnosis:
Non proliferative DR:
Mild, moderate, or severe with microvascular changes limited to the retina
Microaneurysm
Retinal hemorrhages
Venous beading
Retinal edema
Hard exudates
Proliferative DR:
New blood vessels grow on the surface of the retina, optic nerve, or iris;
neovascularization
Diabetic Macular edema:
Central retinal swelling; reduces foveal center visual acuity.
Treatment:
Acute visual changes → Emergent referral to eye doctor.
Urgent referral for all other cases.
Glucose Control
SCREENING!!!!!!
Retinal Detachment
-Physiologic and anatomic mechanisms of retinal attachment are overcome and the retina separates from the underlying retinal pigment epithelium.
Can be caused by trauma/injury, previous ocular surgery, nearsightedness, diabetes, sickle cell (via increased traction on the retina.
S/S:
Monocular decreased visual function
Shadow or curtain descending over the eye.
Cloudy or smoky vision
Floaters
Momentary flashes of light.
Diagnostic:
Fundoscopic Exam → billowing or tentlike elevation of the retina.
Appears gray
Tears/holes best seen with indirect ophthalmoscopy.
Treatment:
Urgent referral (within 24 hours)
Surgery