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Urgent and Emergent Eye Topic Chart
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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)
Papillitis w/hyperemia of disc, blurring of disc margins, distended veins (1/3 of pts)
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)
Topical antibiotics (Erythromycin, trimethoprim-polymyxin B, Ciprofloxacin)
Cycloplegics if large (cyclopentolate, homatropine)
Foreign body that cannot be removed (this isn’t always an emergent referral)
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
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
Tell patient to return promptly for increased pain, redness or impaired vision
Refer: urgently if FB can’t be removed or corneal infection suspected
Corneal opacity, infiltrate, ulceration
Abx eye gtts (fluoroquinolone) applied hourly for 24-48 hours x 2 weeks
Herpes Zoster Opthalmicus Varicella Zoster reactivation within the trigeminal ganglion/nerve
Vesicular eruption along the dermatome
Vesicular lesions on the nose (Hutchinson’s sign) indicate high risk of HZO
Anterior uveitis, increased IOP, nerve palsies, retinal necrosis, corneal scarring are common sequelae
Drug hypersensitivity reactions (Fluoroquinolones, Bisphosphonates, Immunotherapy)
Cornea may be slightly cloudy
Pupil usually small and may become irregular (miosis)
Inflammatory cells and flare within the aqueous of anterior chamber (hypopyon)
Includes the iris (iritis) or ciliary body (cyclitis) or both (iridocyclitis)
Wednesday, April 5, 2023 8:06 AM
Immunotherapy)
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
If GCA use high dose corticosteroids (dx confirmed with temporal artery biopsy)
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
Refer to ophthalmologist
Vitreous Hemorrhage Extravasation of blood into one of the spaces formed within and around the vitreous body
Orbital Cellulitis Infection involving the contents of the orbit (fat and ocular muscles)
Sometimes need anaerobic coverage (metronidazole)
*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)
Diffuse redness or violaceous discoloration
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
**Untreated results in severe and permanent vision loss within hours to days after onset. Refer emergently Retinal Detachment
Traction detachment: vitreoretinal adhesions mechanically pull the retina from the retinal pigment layer. Most common cause: proliferative DM retinopathy
If detachment includes the macula/fovea there is an afferent pupil defect and
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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