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Urgent and Emergent Eye Topic Chart

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2020/2021

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Disease
Cause
Symptoms
Diagnosis
Treatment
Picture
Notes
Optic Neuritis
Ischemic optic neuropathy (Giant Cell
Arteritis)
Infection (meningitis, encephalitis, syphilis)
(Viral)
Develops between 20
-
40 (mean age of 30)
most are female (2/3rds)
Patho: T cell activation > release of
cytokines and other inflammatory agents >
edema in the myelinated nerve sheaths >
myelin breakdown
Pain eye movements
Unilateral (monocular) loss
of vision
developing over
hours to a few days
Decreased color vision
Visual field loss (usually
central)
+ afferent pupillary defect(if
other eye not involved)
Papillitis w/hyperemia of
disc, blurring of disc
margins, distended veins
(1/3 of pts)
Refer to ophthalmology
MRI of brain and orbits
*brain MRI advisable in every
patient with a first attack of optic
neuritis due to chance of multiple
sclerosis, in those whose vision
recovery doesn’t occur, or there
are atypical features (continued
deterioration of vision or
persisting pain after 2 wks)
Lumbar Puncture: not essential
but considered in atypical cases
Other testing: erythrocyte
sedimentation rate, ANA (if
relevant clues to an alte rnative dx)
IV corticosteroids (methylprednisolone)
-
first
line
Immunomodulatory therapies (immune
globulin)
Can follow with oral prednisone (usually if
vision worse than 20/100) but not common
practice
Refer urgently for ophthalmologic and/or
neurologic assessment **Vision usually
improves over 2
-
3 weeks
Corneal
Abrasion
Trauma (fingernails, paws, branches, foreign
body, contact lenses)
Severe pain/FB sensation
Photophobia
Erythema
Exclude penetrating trauma or
infectious infiltrate
through H&P
Get visual acuity FIRST
Analgesia (proparacaine or
tretracaine) if needed then
fluorescein stain exam
Topical antibiotics
(Erythromycin,
trimethoprim
-
polymyxin B, Ciprofloxacin)
Cycloplegics if large (cyclopentolate,
homatropine)
Daily f/u
until healed
Tetanus prophylaxis
Pain control
(NSAIDs, Opioids)
Emergent Referral
Corneal infiltrate, white spot, or opacity
suggestion ulceration
Foreign body that cannot be removed
(this isn’t always an emergent referral)
Hypopyon (pus in the anterior chamber)
Urgent Referral
A larger epithelial defec t
Purulent discharge
A drop in vision of mo re than one to two
lines on a Snellen chart
An infant or child with p ersistent
discharge or unwillingness to keep the
eye open
Corneal abrasion that has not heale d
after three to four days
Corneal
Foreign Body
"something in my eye"
FB under eyelid
: instill anesthetic
(proparacaine 0.5%) and evert the
lid > If FB present can remove by
passing a wet sterile cotton tip
applicator over it
Corneal FB
: examine the eye with
slit lamp or with a hand flashlight,
using oblique illumination > FB
may be made more apparent by
instilling fluorescein > Removed
with a sterile wet cotton tipped
applicator or hypodermic needle
or burr > Bacitracin oint should
then be instilled
Test visual acuity before treatment
Once FB removed cornea starts healing within
24 hours
Tell patient to return promptly for increased
pain, redness or impaired vision
Refer
: urgently if FB can’t be removed or
corneal infection suspected
* Do not give anesthetic gtts to patient
because they are toxic to the corneal
epithelium and can lead to further injury
without patient knowing
*consider intraocular FB if patient gives
history of something hitting the eye
(usually by hammering on metal or using
grinding equip) and no corneal FB is seen,
a corneal or scleral wound is present, or
marked vision loss or media opacity. Refer
emergently to ophthalmologist
Corneal Ulcer
Bacteria
(Staph, Strep, Pseudomonas)
Viruses
(HSV, adenovirus)
Fungal (rare)
Vitamin A deficiency
Pain
Photophobia
Decreased vision
Discharge
FB sensation
Corneal infiltrate (round,
white spot)
Conjunctival hype remia
Meiosis
Chemosis
Fluorescein stain and slit lamp
exam
May need cultured
Cycloplegics
Bacterial
: moxifloxacin (small ulcers) or
tobramycin and cefazolin (significant ulcers)
HSV: ganciclovir, valacyclovir, or acyclovir
Fungal
: natamycin e or amphoter icin B
Bacterial
Keratitis
Improper contact lens wear (greatest risk
factor)
Dry ocular surface
Topical corticosteroid use and/or
immunosuppression
FB sensation
Trouble keeping eye open
(sign of active corneal
process)
Corneal opacity, infiltrate,
ulceration
Red eye
Photophobia
Mucopurulent d/c
Limbic flushing
Mostly clinical
Can get corneal scrapings for
culture and gram stain (performed
by ophthalmologist)
Abx eye gtts
(fluoroquinolone) applied hourly
for 24
-
48 hours x 2 weeks
Cycloplegic gtts
Don’t patch eye
*warrants evaluation by an
ophthalmologist same day
HSV Keratitis
HSV
-
1 or HSV
-
2
Viral latency (trigeminal ganglion)
Can be reactivated by stress, trauma,
fever, UV exposure, and other infections
Unilateral
Pain
Photophobia
Visual blurring
Watery discharge
Conjunctival inj ection near
the limbus
(ciliary flush)
Dendritic lesion
Usually clinical
Three types of testing: Viral
culture, detection of viral antigen
(ELISA/ELVIS), detection of viral
DNA (PCR)
Topical antiviral agents
(Ganciclovir, Acyclovir)
Oral antivirals
(Acyclovir)
Use of topical glucocorticoids are effective but
need to used with caution (best done by
ophthalmologist)
Herpes Zoster
Opthalmicus
Varicella Zoster reactivation
within the
trigeminal ganglion/nerve
Frontal branch
most frequently involved
Headache, malaise, fever
Unilateral pain/tingling in
affected eye/forehead/scalp
Vesicular eruption along the
dermatome
Vesicular lesions on the nose
(
Hutchinson’s sign
) indicate
high risk of HZO
Conjunctivitis
Lid droop
Corneal involvem ent
(keratitis)-Corneal dendrites
Anterior uveitis, increased
IOP, nerve palsies, retinal
necrosis, corneal scarring
are common sequelae
Antivirals
(oral or topical)
Topical steroid drops
Anterior
Uveitis
Inflammation of uveal tract
Infections- Bacterial, viral, fungal, and
parasitic (HSV, CMV, Toxoplasmosis,
Syphilis, West Nile)
Systemic immune-mediated disease (40%)
Inflammatory disease (Ankylosing
spondylitis, Reactive arthritis,
Inflammatory Bowel Disease)
-
Drug hypersensitivity reactions
(Fluoroquinolones, Bisphosphonates,
Immunotherapy)
-
Unilateral,
deep, aching pain
Decrease in visual acuity
Ciliary injectio n or diffusely
red
Cornea may be slig htly
cloudy
Pupil usually small and may
become irregular (miosis)
Photophobia (consensual)
Slit lamp and dilated fundus exam
Keratitic precipitates (white
cells on endothelium)
Inflammatory cells and flare
within the aqueous of
anterior chamber
(hypopyon)
Refer to ophthalmology
Infectious: antiviral agents, abx
Noninfectious: topical glucocorticoi d
(prednisolone); mydriatics (scopolamine)
Includes the iris (iritis) or ciliary body
(cyclitis) or both (iridocyclitis)
Urgent & Emergent Eye
Wednesday, April 5, 2023 8:06 AM
Urgent Emergent Eye Page 1
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Disease Cause Symptoms Diagnosis Treatment Picture Notes Optic Neuritis • **Multiple Sclerosis Ischemic optic neuropathy (Giant Cell Arteritis)

Infection (meningitis, encephalitis, syphilis) (Viral)

  • Develops between 20-40 (mean age of 30)
  • most are female (2/3rds) Patho: T cell activation > release of cytokines and other inflammatory agents > edema in the myelinated nerve sheaths > myelin breakdown
  • Pain eye movements Unilateral (monocular) loss of vision developing over hours to a few days
  • Decreased color vision Visual field loss (usually central)
  • afferent pupillary defect (if other eye not involved)

Papillitis w/hyperemia of disc, blurring of disc margins, distended veins (1/3 of pts)

  • Refer to ophthalmology
  • MRI of brain and orbits *brain MRI advisable in every patient with a first attack of optic neuritis due to chance of multiple sclerosis, in those whose vision recovery doesn’t occur, or there are atypical features (continued deterioration of vision or persisting pain after 2 wks) Lumbar Puncture: not essential but considered in atypical cases

Other testing: erythrocyte sedimentation rate, ANA (if relevant clues to an alternative dx)

IV corticosteroids (methylprednisolone)-first line

Immunomodulatory therapies (immune globulin)

Can follow with oral prednisone (usually if vision worse than 20/100) but not common practice

Refer urgently for ophthalmologic and/or neurologic assessment **Vision usually improves over 2-3 weeks

Corneal Abrasion Trauma (fingernails, paws, branches, foreign body, contact lenses)

  • Severe pain/FB sensation
  • Photophobia
  • Erythema Exclude penetrating trauma or infectious infiltrate through H&P
  • Get visual acuity FIRST Analgesia (proparacaine or tretracaine) if needed then fluorescein stain exam

Topical antibiotics (Erythromycin, trimethoprim-polymyxin B, Ciprofloxacin)

Cycloplegics if large (cyclopentolate, homatropine)

  • Daily f/u until healed
  • Tetanus prophylaxis
  • Pain control (NSAIDs, Opioids) Emergent Referral Corneal infiltrate, white spot, or opacity suggestion ulceration

Foreign body that cannot be removed (this isn’t always an emergent referral)

  • Hypopyon (pus in the anterior chamber) Urgent Referral
  • A larger epithelial defect
  • Purulent discharge A drop in vision of more than one to two lines on a Snellen chart

An infant or child with persistent discharge or unwillingness to keep the eye open

Corneal abrasion that has not healed after three to four days

Corneal Foreign Body

  • "something in my eye" FB under eyelid: instill anesthetic (proparacaine 0.5%) and evert the lid > If FB present can remove by passing a wet sterile cotton tip applicator over it

Corneal FB: examine the eye with slit lamp or with a hand flashlight, using oblique illumination > FB may be made more apparent by instilling fluorescein > Removed with a sterile wet cotton tipped applicator or hypodermic needle or burr > Bacitracin oint should then be instilled

  • Test visual acuity before treatment Once FB removed cornea starts healing within 24 hours

Tell patient to return promptly for increased pain, redness or impaired vision

Refer: urgently if FB can’t be removed or corneal infection suspected

  • Do not give anesthetic gtts to patient because they are toxic to the corneal epithelium and can lead to further injury without patient knowing *consider intraocular FB if patient gives history of something hitting the eye (usually by hammering on metal or using grinding equip) and no corneal FB is seen, a corneal or scleral wound is present, or marked vision loss or media opacity. Refer emergently to ophthalmologist Corneal Ulcer • Bacteria (Staph, Strep, Pseudomonas)
  • Viruses (HSV, adenovirus)
  • Fungal (rare)
  • Vitamin A deficiency
    • Pain
    • Photophobia
    • Decreased vision
    • Discharge
    • FB sensation Corneal infiltrate (round, white spot)
  • Conjunctival hyperemia
  • Meiosis
  • Chemosis Fluorescein stain and slit lamp exam
  • May need cultured
    • Cycloplegics Bacterial: moxifloxacin (small ulcers) or tobramycin and cefazolin (significant ulcers)
  • HSV: ganciclovir, valacyclovir, or acyclovir
  • Fungal: natamycine or amphotericin B Bacterial Keratitis Improper contact lens wear (greatest risk factor)
  • Dry ocular surface Topical corticosteroid use and/or immunosuppression
  • FB sensation Trouble keeping eye open (sign of active corneal process)

Corneal opacity, infiltrate, ulceration

  • Red eye
  • Photophobia
  • Mucopurulent d/c
  • Limbic flushing
    • Mostly clinical Can get corneal scrapings for culture and gram stain (performed by ophthalmologist)

Abx eye gtts (fluoroquinolone) applied hourly for 24-48 hours x 2 weeks

  • Cycloplegic gtts
  • Don’t patch eye *warrants evaluation by an ophthalmologist same day HSV Keratitis • HSV-1 or HSV- 2
  • Viral latency (trigeminal ganglion) Can be reactivated by stress, trauma, fever, UV exposure, and other infections
  • Unilateral
  • Pain
  • Photophobia
  • Visual blurring
  • Watery discharge Conjunctival injection near the limbus (ciliary flush)
  • Dendritic lesion
    • Usually clinical Three types of testing: Viral culture, detection of viral antigen (ELISA/ELVIS), detection of viral DNA (PCR)
  • Topical antiviral agents (Ganciclovir, Acyclovir)
  • Oral antivirals (Acyclovir) Use of topical glucocorticoids are effective but need to used with caution (best done by ophthalmologist)

Herpes Zoster Opthalmicus Varicella Zoster reactivation within the trigeminal ganglion/nerve

  • Frontal branch most frequently involved
    • Headache, malaise, fever Unilateral pain/tingling in affected eye/forehead/scalp

Vesicular eruption along the dermatome

Vesicular lesions on the nose (Hutchinson’s sign) indicate high risk of HZO

  • Conjunctivitis
  • Lid droop Corneal involvement (keratitis)-Corneal dendrites

Anterior uveitis, increased IOP, nerve palsies, retinal necrosis, corneal scarring are common sequelae

  • Antivirals (oral or topical)
  • Topical steroid drops Anterior Uveitis
  • Inflammation of uveal tract Infections- Bacterial, viral, fungal, and parasitic (HSV, CMV, Toxoplasmosis, Syphilis, West Nile)
  • Systemic immune-mediated disease (40%) Inflammatory disease (Ankylosing spondylitis, Reactive arthritis, Inflammatory Bowel Disease)

Drug hypersensitivity reactions (Fluoroquinolones, Bisphosphonates, Immunotherapy)

  • Unilateral, deep, aching pain
  • Decrease in visual acuity Ciliary injection or diffusely red

Cornea may be slightly cloudy

Pupil usually small and may become irregular (miosis)

  • Photophobia (consensual) Slit lamp and dilated fundus exam Keratitic precipitates (white cells on endothelium)

Inflammatory cells and flare within the aqueous of anterior chamber (hypopyon)

  • • Refer to ophthalmology
    • Infectious: antiviral agents, abx Noninfectious: topical glucocorticoid (prednisolone); mydriatics (scopolamine)

Includes the iris (iritis) or ciliary body (cyclitis) or both (iridocyclitis)

Urgent & Emergent Eye

Wednesday, April 5, 2023 8:06 AM

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  • Syndromes confined to the eye Posterior Uveitis Same as above Includes the choroid/retina (choroiditis, chorioretinitis, retinitis, vitritis)
  • Gradual vision loss
  • Minimally inflamed eye
  • Floaters
  • Bilateral common Slit lamp and dilated fundus exam inflammatory cells in the vitreous humor and active chorioretinal inflammation
  • • Infectious: antiviral agents, abx Noninfectious: systemic/periocular/intravitreal corticosteroid therapy
  • Pupil dilation usually not necessary **Refer both types emergently especially if extreme pain or vision loss Central Retinal Artery Occlusion DM, hyperlipidemia and HTN make you more susceptible

Embolism from carotid artery atherosclerosis (most common)

Consider giant cell arteritis in patients over 50

Patho: Occlusion of retinal arteries from emboli (carotid atherosclerosis or heart) or development of thrombus > ischemia of retina distal to occlusion

Sudden, painless monocular vision loss

May be preceded by Amaurosis fugax

  • Afferent pupillary defect Pallid swelling of retina with a cherry red spot at macula
  • Fundoscopy
  • Fluorescein angiography Some labs/imaging (r/o underlying cause) Screen for HTN, glucose, fasting lipid profile, ESR/C- reactive protein (vasculitis)
  • Find emboli source Carotid US, ECG, Echocardiogram
  • Lay patient flat
  • Ocular massage
  • O IV acetazolamide or anterior chamber paracentesis

If GCA use high dose corticosteroids (dx confirmed with temporal artery biopsy)

  • Refer emergently Amaurosis Fugax Ischemia (papilledema, optic neuropathy, artery occlusion, carotid artery disease, GCA)
  • Retinal vein occlusion
  • Retinal vasospasm Optic nerve compression (tumors, trauma, Graves’ ophthalmopathy)
  • Increased IOP Monocular, transient vision loss described as a rapid fading of vision like a “curtain descending over the eye.”
  • Lasts seconds to hours Disc swelling suggests event involving the optic nerve (ischemia or inflammation)

Retinal whitening often reflects ischemia (branch or central retinal artery occlusion)

Retinal hemorrhages, tortuous veins, and neovascularization may reflect reduced retinal arterial flow and venous stasis (severe carotid stenosis)

Retinal Vein Occlusion Patho: Occlusion from either a thrombus or compression by a crossing retinal artery > back up of venous blood flow > vessel hemorrhage into vitreous and possible limited arterial flow into capillary beds > ischemia

Risk factors: Age, HTN, DM, Smoking, Obesity, Hypercoagulable state, Glaucoma, Retinal vessel abnormalities

Unilateral scotoma or visual field deficit

  • May be gradual or sudden
  • Painless Fundus examination: retinal hemorrhage, optic disk edema, dilated retinal veins, and possibly cotton wool spots
  • Vision may return
    • Mostly clinical Fluorescein angiography and coherence tomography can confirm dx
  • Hypercoagulable workup Screened for cardiovascular risk factors

Refer to ophthalmologist

  • Laser photocoagulation
  • Inject meds into retina

Vitreous Hemorrhage Extravasation of blood into one of the spaces formed within and around the vitreous body

  • Retinal tears
  • Retinal vein occlusions
  • Trauma
  • Systemic disorders (DM, HTN)
  • Diabetic/hypertensive retinopathy Sudden, painless loss or deterioration of vision in affected eye
  • No redness or inflammation Red reflex is hazy, faint, or black
  • May resolve on own Partial or total vitrectomy (if absorption of blood doesn’t occur or if blood clots)

Orbital Cellulitis Infection involving the contents of the orbit (fat and ocular muscles)

  • Often arises from the paranasal sinuses
  • S. aureus & Streptococci most common
  • More common in children Ocular pain especially with eye movement
  • Restricted mobility of EOMs
  • Proptosis
  • Lid erythema/edema
  • Chemosis
  • Fever
  • Decreased acuity
  • Afferent pupillary defect
  • Leukocytosis
    • Orbit/sinus CT scan
    • Blood cultures, CBC Culture of sinus drainage if concomitant sinusitis
  • Hospitalize immediately Broad spectrum IV abx that includes coverage of MRSA Vancomycin PLUS Ceftriaxone or Cefotaxime

Sometimes need anaerobic coverage (metronidazole)

  • May require surgical drainage if abscess forms Complications: subperiosteal abscess, orbital abscess, vision loss, cavernous sinus thrombophlebitis, brain abscess

MEDICAL EMERGENCY

*The superior and inferior orbital veins drain blood directly into the cavernous sinus making it easier for infection to pass readily from the orbit to intracranial structures Ocular Chemical Burns Alkali Burns (Worse)- Liquefactive necrosis, denatures proteins & collagen, causes thrombosis of vessels

Acid Burns- Coagulative necrosis > protective barrier > less penetration (except hydrofluoric acid)

  • Decreased vision
  • Moderate to severe pain
  • Photophobia
  • Erythema
    • Check MSDS
    • Check Ph (neutral pH is 7.0-7.4) Immediate irrigation - At least 2 liters (6 liters is better)
  • Stain eye to identify ulceration Abx gtts (Erythromycin, polymyxin- trimethoprim)
  • Refer to ophthalmology Scleritis Painful, destructive, and potentially blinding inflammatory disorder of sclera
  • Autoimmune (RA, SLE), syphilis, gout Patho: Inflammatory invasion and immune complex deposition in vessels > fibrinoid necrosis, thrombotic occlusion of vessels and inflammatory response in the sclera

Diffuse redness or violaceous discoloration

  • Vascular engorgement
  • Severe, boring eye pain
  • Tenderness of globe
  • Photophobia
    • Refer to ophthalmology Systemic therapy - Oral NSAIDs or corticosteroids (1st line) - Immunosuppressive drugs (second line)

Acute Angle Closure Glaucoma Primary angle-closure: patients are anatomically predisposed; there are no identifiable secondary causes (Asian descent, hyperopia)

Secondary angle-closure: secondary process is responsible for narrowing or closure of angle (mass, hemorrhage, iritis)

Risk factors: FHx, Age>60, Female, Hyperopia, Mydriasis, Asian

Patho: Drainage pathway is narrowed or closed > inadequate drainage of the aqueous humor > increased IOP and damage to the optic nerve/ganglion cell axons

Acute, extremely painful, red eye with blurred vision

Corneal edema (hazy/steamy cornea), halos around lights, peripheral vision loss

N/V, ha, fixed mid-dilated pupil

Tonometry: Measure IOP (usually >30 mmHg) during the attack

  • Gonioscopy Pressure lowering agents- Timolol, apraclonidine, pilocarpine
  • Acetazolamide PO/IV If these fail a laser can be used to create a hole in the peripheral iris (iridotomy or iridectomy)

**Untreated results in severe and permanent vision loss within hours to days after onset. Refer emergently Retinal Detachment

  • Generally occurs in people >50; M>F Rhegmatogenous (most common): vitreous fluid gains access to the subretinal space through a break in the retina

Traction detachment: vitreoretinal adhesions mechanically pull the retina from the retinal pigment layer. Most common cause: proliferative DM retinopathy

  • Floaters
  • Flashing lights (photopsia) Curtain spreading across field of vision or sudden onset of visual loss in one eye

If detachment includes the macula/fovea there is an afferent pupil defect and

  • Fundoscopic exam of dilated eye Keep pt supine with head turned toward the side of detachment

Uncomplicated detachment may be treated with pneumatic retinopexy then sealed by laser photocoagulation or cryotherapy

Complicated detachment may need a vitrectomy, direct manipulation of retina, and internal tamponade of the retina with air, gas or silicone oil

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