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OCULAR EMERGENCIES EYE EXAMINATION History Past ocular trauma, surgery, eye related problems Preexisting visual impairment, glassess, contacts Onset and description of current problems Work exposure (grinding, welding, etc), eye treatment General medical health Eye questions ......... changes in vision, flashers, floaters, black spots redness discharge foreign body sensation photophobia Physical Examination General Inspection Trauma Anatomy Basilar skull # Orbital # Face Globe disruption: limited exam Visual Acuity and Visual Fields MUST always be measured and documented (legal issues) Use glasses or pin hole Snell chart - count fingers - hand motion - light perception Can use near card in trauma room Document clearly PINHOLE: corrects refractive error Vision corrects with pinhole: not worried Vision doesn't correct: retinal problem, vitreous problem, korneal, lens Pupils PERLA Afferent pupilary defect (optic nerve abnormality) Poorly reactive could be due to previous eye surgery or trauma, miotics (pilocarpine), or mydriatics (atropine), or cyclopentolate EOM Paralysis can be seen in many lesions including diabetes, intracranial aneurysm/tumors, intraorbital masses, myasenia gravis, demyelinating diseases, intracranial inflammatory lesions, sphenoid sinusitis, trauma Lids/Ocular Adnexa Evaluate the position, contour, and color of the lids and periocular areas. Check for swelling, discharge.

Anterior Segment Includes cornea, conjunctiva, anterior chamber, iris, lens Evaluated with slit lamp Examine anterior chamber for wbc (inflam), rbc.s (hyphema), or increased protein in aqueous fluid (flare = "fog"phenomenon) Blue light used to look for corneal or conjunctival epithelial defects after putting in flouroscein dye. Intraocular Pressure Measure when concerned about gluacoma (hyphema or iritis) or low pressure (ruptured globe) Use tonopen, tonometer,dodmann applanation Normal IOP ranges from 10 - 21 Anesthetize the cornea b/f measurement Fundus Optic nerve, retina, retinal vessels Contraindication for dilation: iris-supported intraocular lens, untreated narrow angle glaucoma Dilation: Mydiacyl 1%, Phenylephrine 2.5% Orbit Orbital symmetry, proptosis Palpate orbital rim Think about orbital floor or wall fractures in blunt trauma Examine occular motility for entrapment Xrays: AP and Water's view CT Proptosis ddx: orbital hemorrhage, emphysema, edema, tumors Differential diagnosis of unilateral Proptosis Retroorbital hematoma Retroorbital abscess Retroorbital tumor C/I TO DILATING A PUPIL Hx of Glaucoma Iris of Bombay Ocular Trauma Retrorbital emphysema Edema Differential diagnosis of bilateral Proptosis Hyperthyroidism Lymphoma Metastasis Lacrimal gland inflammation Leukemias: kids Metastatic neuroblastomas: kids Differential diagnosis of a RED EYE Conjunctivitis, conjunctival FB Keratitis, corneal ulcer, corneal fb, UV keratitis Episcleritis

Scleritis Uveitis Acute angle closure glaucoma OCULAR TRAUMA ORBIT AND LID CONTUSION Echymosis, swelling of orbits and surrounding tissues Most important thing is to look for other injuries Examine under eyelids, obtain visual acuity Ice, elevation, NSAIDs or tylenol; See MD for increase in symptoms ORBITAL WALL FRACTURES Blunt force, acute rise in intraorbitral pressure, prolapse of orbital soft tissues (usually into the maxillary sinus because the orbital floor is the weakest orbital wall) Orbital floor fracture/Blow out fracture Entrapment of the inferior rectus, inferior oblique, orbital fat and connective tissue --------------> enopthalmos, ptosis, diplopia, limitation of upward gaze MAY have infraorbital nerve sensory loss if associated inferior orbital rim # Subcutaneous orbital emphysema may be palpable LOOK for associated globe injury: 10 - 25% Tear-drop sign: bulge extending from the orbital floor into the maxillary sinus on Xray, and A/F level in maxillary sinus are indirect signs of orbital floor fractures Surgical repair: only for persistent diplopia or cosmetic concerns and is not usually performed until 7 - 10 days to allow swelling to subside Avoid blowing nose and valsalva to minimize orbital emphysema Maxillary sinusitis: antibiotics, ice packs, decongestants F/U with plastics Antibiotic prophylaxis only if concurrent sinusitis Medial orbital wall Fractures through the ethmoid bone and enters the ethmoid sinus Orbital emphysema (because of ethmoid air sinuses) and epistaxis Diplopia from medial rectus impingement can occur Orbital emphysema should prompt search for associated injury Orbital emphysema can be significant (rarely): compression of optic nerve and acute visual loss; usually resolves on own, abx coverage not indicated unless fracture involves infected sinus

RETRO-ORBITAL HEMATOMA HEmorrhage in the potential space behind or around the eye Significant hemorrhage leads to rise in intraorbital pressure that is transmitted to globe and optic nerve ; central retinal artery occlusion possible ("compartment syndrome") SIGNS Proptosis Decreased visual acuity Afferent pupillary defect Increased IOP Decreased extraocular movement Orbital CT will demonstrate the hematoma Immediate opthamology consult warranted Decrease intraocular pressure with carbonic anhydrase inhibitor, beta-blocker topically, iv mannitol Lateral canthotomy is definitive tx and should be done in ED if indicated Prep the lateral canthus site Inject lidocaine + epinephrine Mosquito clamp to lateral canthus Horizontal 1cm incision with cutting scissors Release the lateral canthal (palpebral) ligament CHEMICAL BURNS TO CORNEA/CONJUNCTIVA True ocular emergency Alkalis: drain cleaners, detergents, solvents, lime ------> liquefaction necrosis that penetrates and dissolves tissues until the alkaline agent is removed Acids: coagulation necrossis, less severe because precipitation of tissue proteins limits injury General rule: alkaline with pH < 12 and acid with pH > 2 are thought not to cause significant injury BUT concentration and time of contact are important factors also Immediate, copious irrigation should be started at scene and continued for at least 30 min before any attempt at transport (do NOT interrupt irrigation to transport) Severity: degree of corneal clouding and scleral whitening Long-term complications: perforation, scarring, glaucoma, neovascularization of the cornea, adhesions of the lids to the globe (symblepharon), cataracts, retinal damage ED Topical anesthetic Manual lid retraction to r/o retained chemical particles (remove with swab) Insert a Morgen lens and irrigate 2L NS After irrigation, wait test pH, wait 15 min and retest if OK Irrigate until the tear film pH is neutral 7.40

Examination after irrigation: topical aneshtetic, look carefully for retained material especially in fornicies, check IOP (esp important in alkali burns) Update tetanus Discuss with opthamology to arrange f/u and ask what they want to treat with Cycloplegic (avoid phenylephrine) Topical antibiotics Pain management Artificial tears q2hr

MISC SOLVENTS/IRRITANTS Treat all exposures as acids/alkalis: assume the worst and irrigate like hell Detergents: conjunctival irritation, may cause anterior chamber inflammation: tx as corneal abrasion Aerosol exposures: irrigate, check pH, topical antibiotics, pain control, consider intraocular foreign body with propellants Management of ocular superglue exposures: Immediate irrigation if possible Artificial tears qid Patch both eyes Arrange optho f/u Superglue will dissolve with time; if eyelids inverted may need surgical intervention; consult opthamology regardless THERMAL BURNS More common to affect eyelids than globe because of reflex blinking and Bell's phenomenon Superficial eyelid burns: irrigation, topical antibiotic ointment 2nd or 3rd degree eyelid burns: opthamology consult Hot liquid splashes and ashes to cornea: superficial corneal injury and treat as corneal abrasion Molten metals and other hot objects may result in globe perforation Polysporin bid to eyelid burns

RADIATION BURNS (ULTRAVIOLET KERATITIS, SOLAR KERATITIS) Ultraviolet light: sun lamps, tanning booths, high-altitude env, welder's arc Ultraviolet light is directly toxic to the cornea Latency of 6 - 12 hrs before symptoms Symptoms Ocular pain FB sensation Tearing Photophobia Signs Blephorospasm Decreased visual acuity

Conjunctival infection Diffuse punctate keratitis (often with a discrete lower border defining the cornea protected by the inferior lid) Management Tx: short acting cycloplegic, topical antibiotic ointment, eye patching for comfort, oral narcotics, opthamology f/u in 24hrs NEVER prescribe topical anesthetic drops ------> retards healing and can lead to corneal ulcer formation

CORNEAL ABRASIONS Pathophysiology Cornea has abundant nerve supply thus very sensitive Cornea heals quickly thus improvement expected rapidly Small abraisons heal in 24hrs Moderate in 48hrs Large in 72hrs Symptoms Ocular pain FB sensation Photophobia Blurry vision Signs Decreased visual acuity Blepharospasm Conjunctival injection Epithelial defect with fluerescein staining Must LOOK for FB Management Topical anesthetics to aid exam and decrease pain No routine patching (can use if very large and it seems to help) No routine abx (consider if very large) Oral analgesics: ibuprofen, few percocet Topical NSAIDS: Acular 0.5% one gtt qid X 3/7 (expensive $45) or voltaren Cycloplegics: two drops of 5% homoatropine in ED, could give prescription after but the duration of this is 10-48hrs thus well on the way to healing. Avoid contact lenses Update tetanus Small: no follow up unless problems Large: f/u in 24-48hrs in ED or optho Indications for opthamologic consultation

Very large corneal abraison Center of visual access Failure to improve in 24-48hrs De-epithelialization = when patient blinks they remove the new corneal surface thus preventing or delaying healing; use ++ artificial tears and refer to optho Evidence re Patching Kaiser P. Opthamology 1995. 102: 1936-1942. Mydriatric, abx ointment, then randomized to patch Days to heal: 2.3 no patch vs 2.6 patch (significant) Pain scale: 1.8 no patch vs 2.53 patch (signficant) Subgroup of large abraisons > 10 mm: "trend" towards faster healing with patching Campanile et al. J of Emerg Med 1997. 15 (6): 769-774. % healed at 24hrs: 97% no patch, 84% with patch

Evidence re Antibiotic prophylaxis King J. Can Fam Phys 39: 2349-2352. 1993. Corneal abraisons, FB, minor burns, UV keratitis Prospective observational study F/u at 1-3 days (90%) 0.7 % had a corneal or conjunctival infection Evidence re topical NSAIDS Szucs. Annals 2000. 35(2) Voltaren 0.1% vs placebo drops Pain scale decreased 3.1 points vs 1.0 with placebo Kaiser. Opthamology 1997. 104(8) Ketorolac vs placebo Decreased pain at 24hrs Decreased photophobia, FB sensation No delay in healing Earlier return to work (½ day) CORNEAL FOREIGN BODIES Symptoms FB sensation Ocular pain Tearing +/- blurry vision Signs Blepharospasm FB on cornea Conjunctival +/- decreased acuity Underlying corneal abraison

Removal Cotton tip Irrigation Needle: 25 guage Commercial eye spud CONSIDER intraocular FOREIGN BODIES High-speed drills, saws, grinders, pounding objects, explosions Dye streaming, extruded ocular contents, pupillary defect, Orbital Xray if radiopaque, orbital CT other option Corneal Rust Rings Occurs with oxidization after contact with a metal corneal FB Must remove metallic rust particles Rust stain: attempt early removal or recheck in 24-48hrs as it may "migrate" to the surface as the cornea reepithelizes Removal: needle, burr Manage after as a corneal abraison Referral for very large or deep rust rings or problems removing

CONJUNCTIVAL FOREIGN BODY Attempt removal before local anesthetic then patient will be able to tell you it is gone! Make sure you ever both eyelids and do a double eversion! Persistent FB sensation and you can't find anything Wait 24 hrs Optho referral if doesn't improve (you can rarely have things hidden way up where you can't see) Unique complicaiton of perilimbal foreign body Can trigger a pterygium = conjunctiva grows onto the corneal surface

INTRAOCULAR FOREIGN BODIES Small intraorbital and intraocular FB can occur with any perforating injury Difficult to diagnose SUSPECT with grinding, sanding, drilling, hammering, explosions Investigate based on HISTORY alone; physical may be normal Xray, U/S, CT for diagnosis Xray: metal, or glass U/S: wood CT: everything Orbital CT probably the most useful MRI contraindicated if metallic FB suspected Siderous Oxidation: late complication of iron containing FB that can lead to visual loss Chalcosis: sterile inflammatory reaction to copper containing compounds that may require removal of offending agent

History Grinding, sanding, drilling, hammering, explosion Felt a "twinge" in my eye but it doesn't hurt now (compared to corneal or conjunctival FB which cause ongoing pain) Signs May be none Distorted pupil Extruding intraocular contents Streaming of dye on the cornea Localized collection of blood over the sclera Management as per globe penetration Opthamology consult NPO Eye shield Antibiotics Removal: depends on what it is; organic FB are removed b/c of risk of infection; inorganic (metal, glass, plastic) may be left b/c removal may cause more damage

SUBCONJUNCTIVAL HEMORRHAGE Rupture of small subconjunctival blood vessel as a result of trauma or valsalva maneuver Can occur spontaneously without apparent cause Should be asymptomatic: pain, diminished visual acuity, photophobia suggest other problem Flat, bright red, smooth, limited to the bulbar conjunctiva, sharply demarcated at the limbus MUST distinguish from bloody chemosis (edema of conjunctiva) which is indicative of more serious globe pathology MUST consider globe rupture with large, circumferential, elevated subconjunctival hemm Bilateral or recurrent subconjunctival hemorrhages may require work up for bleeding diathesis Treatment: cold compress X 24hrs, resolution in 2 - 3 weeks TRAUMATIC HYPHEMA Disruption of blood vessel in iris or ciliary body Blood layers if pt sitting and forms a meniscus with the aqueous humor Size ranges from microscopic hyphema to "eightball" Symptoms Ocular pain Photophobia Blurry vision Signs Decreased visual acuity

Anterior chamber microscopic red cells Anterior chamber hyphema Elevated IOP NO afferent pupilllary defect unless eight ball Complications Elevated intraocular pressure Corneal staining Rebleeding Synechiae Management R/O other ocular injuries List five discharge instructions: Tylenol for pain Avoid aspirin, ibuprofen, antiplatelets Limited activity Avoid reading Avoid valsalva Discuss with optho to arrange followup (they can decide what to treat with if anything): miotics, mydriatics, cycloplegics, steroids, antifibrinolytics (aminocaproic acid) Increased intraocular pressure: discuss with optho; topical beta blocker; add topical alpha agonist or topical carbonic anhydrase inhibitor if needed; oral acetaxolamide or IV mannitol may be used Surgical intervention with raised IOP that isn't responsive to medical mx Case reports of anterior chamber thrombolysis

Rebleeding Major complication, usually 2 - 5 days when the initial clot retracts and loosens There is NO DIFFERENCE in rebleeding rates with inpatient vs outpatient Rx List five predictors of rebleeding (i) poor initial visual acuity (20/200) (ii) large initial hyphyema (covering > 1/3 of anterior chamber) (iii) late presentation (presents > 1 day after injury) (iv) elevated IOP at initial exam Hemoglobinopathies Sickle cell anemia, thalasemia, etc Increased risk for complications RBC in anterior chamber is acidic and hypoxic leading to decreased aqueous humor outflow and rapid rise in IOP Tx: topical beta blockers: leave other antiglaucoma Rx to opthamology (methazolamide may be used instead of acetazolamide) TRAUMATIC IRIDOCYCLITIS Contusion and inflammation of the iris and ciliary body resulting in ciliary spasm Hx: deep eye pain, photophobia, excessive tearing

O/E: perilimbal conjunctival injection (ciliary flush), cells and flare in the anterior chamber, small poorly dilated pupil Treatment Long acting cycloplegics to paralyze the iris and ciliary body (homatropine methylbromide 5% 1 gtt qid X 7 days) Prednisolone acetate 1% may be given to reduce inflammation if there is no improvement in 5 7 days but should be avoided in patients with a corneal epithelial defect (leave to opthamology) Resolution in 1 week MISC ANT CHAMBER/IRIS NONPENETRATING TRAUMA Traumatic mydriasis and miosis Blunt injury may result in either pupillary dilation or constriction May persist for days Must r/o cranial nerve palsy before ascribing to local contusion Permanent mydriasis may result from small radial tears in the pupillary sphincter muscle; pupil margin may be irregular or scalloped, no specific tx Iridodialysis Tearing of the iris root from the ciliary body leading to the formation of a "secondary accessory pupil" Often the cause of a hyphema No specific tx Large tears may need surgery, f/u with optho Anterior Chamber angle recession Blunt injury to ciliary body may cause posterior displacement of the iris increasing the anterior chamber and damaging the trabecular meshwork that drains the aqueous humor Can cause acute glaucoma

CATARACT Lens capsule disruption, dehydrated stroma of lens absorbs fluid, swells, and becomes cloudy Acute glaucoma may develop from blockage of the aqueous humor flow through the pupil necessitating surgery Cataract formation may occur over weeks to months LENS SUBLUXATION AND DISLOCATION Complete disruption of lens zonule fibers may result in complete ant or posterior dislocation Incomplete disruption of lens zonlule fibers results in subluxation MINOR trauma: Marfans's, homocystinuria, tertiary syphilus, other predisposing conditions Hx: monocular diplopia or visual distortion with subluxation and marked visual blurring with dislocation O/E: decreased visual acuity, edge of subluxed lens can be seen when pupil is dilated, iridodonesis is the trembling or shimmering of the iris after rapid eye movements and is a helpful sign of lens dislocation Tx: observation to surgical removal depends on location of dislocated lens and associated eye injury as per immediate opthamology consult

GLOBE RUPTURE Sudden elevation in IOP from blunt trauma may cause scleral rupture Two most common locations are where the sclera is thinnest: (i) insertions of intraocular muscles or (ii) limbus where sclera is thinnest Diagnosis may not be obvious when intraocular contents are seen Symptoms Hx of ocular trauma Ocular pain Blurry vision Signs Extruding ocular contents: brown/black jelly Decreased visual acuity Streaming dye on the cornea Distorted pupil = teardrop pupil Severe bloody chemosis Severe subconjunctival hemorrhage at scleral rupture sits Decreased I.O.P: Hx: eye pain, decreased vision: Tonometry is CONTRAINDICATED if suspecting ruptured globe Management Avoid any maneuver that increased IOP: analgesia, antiemetics Avoid further examination or manipulation of the eye Eye shield to prevent accidental pressure on eye: Fox eye shield or tap a cup over eye (NO gauze over eye b/c it will draw out fluid) NPO Tetanus Do NOT measure IOP IV broad spectrum antibiotics Avoid succinylcholine (ya right!) Consult opthamology: CT, U/S, indirect opthalmoscopy may play a role in occult globe ruptures Succinylcholine, IOP, and globe rupture or penetrating eye injury Globe rupture/penetration listed as contraindication to succinylcholine Succinylcholine increases IOP 1 - 4 min after administration, lasts 7 min Many agents have been tried to prevent incr IOP: nondepolarizing paralytics, diazepam, gallamine, tubocurarine Libonati 1985: 100 patients with penetrating eye injury pretreated with nondepolarizing agent then given succinylcholine -----> NO adverse events NOTE: succinylcholine increaes IOP by 3 - 8 mmHg, blinking increases by 10 - 15 mmHg, coughing/bucking/resisting will increase IOP MORE than succinylcholiine, airway management more important Could use nondepolarizer instead for paralysis but will be paralyzed for 30+ minutes MISCELLANEOUS OCULAR INJURIES

Vitreous hemorrhage: floaters, decreased acuity, manage like a hyphema and refer to optho Retinal tears and detachments: flashers and floaters, decreased acuity, f/u with optho Retinal hemorrhages Preretinal (subhyaloid), superficial retinal, or deep (subretinal) spaces Preretinal hemorrhage: boat shaped Superficial retinal hemorrhage: flame shaped Deep retinal hemorrhage: rounded and grape-purple colorvement Commotio Retinae Decreaed visual acuity or asymptomatic Cloudy whitening of the involved retina that will subside in weeks No specific treatment F/U to ensure that retinal tear or detachment hasn't occurred Optic nerve injuires: avulsion, transection, contusion, compression of optic nerve Suspect with orbital fractures Decreased visual acuity, A.P.D. Orbital CT, r/o retrorbital hematoma Optho consult

EYELID LACERATIONS LOOK for globe rupture and intraocular foreign bodies Simple = ED repair Horizontal or oblique Partial thickness 6-0 or 7-0 nylon Removal in 3 - 5 days Complex = Opthamology or plastics Vertical Full thickness Involving the tarsal plate (correction must be perfect) Involving the lid margins Involving the canalicular system (medial to puncta of lower eyelid) Involving the levator or canthal tendons Lacerations with tissue loss

Through the orbital septum: orbital fat will protrude through septal lacerations into the wound; eyelids have no subcutaneous fat thus the appearance of fat in a lid laceration confirms the diagnosis; HIGH incidence of globe penetration and intraorbital foreign bodies CONJUNCTIVAL LACERATIONS LOOK for intraocular FB or scleral perforations (common) Slit lamp examination to help distinguish superficial versus deep lacerations Small, superficial lacerations: no suturing, heal quickly, topical antibiotics Large (>1cm) or deep: may require repair, consult opthamology CORNEAL AND SCLERAL LACERATIONS Corneal lacerations Signs of full thickness corneal lacerations include loss of anterior chamber depth, teardropshaped pupil caused by iris prolapse through the corneal laceration, blood in the anterior chamber Small lacerations can be difficult to dx: slit - lamp examination may reveal aqueous humor leaking from the corneal wound and is seen as streaming fluorescent dye surrounded by an orange pool of solution Full-thickness corneal lacerations are managed as traumatic globe rupture: avoid eye manipulation, eye shield, NPO, iv antibiotics, antiemetics, optho consult Superficial partial - thickness corneal lacerations: cycloplegic, topical abx, pressure patch if not gaping; to OR for closure if gaping Scleral lacerations Presentation and managment as per blunt globe rupture

COMPLICATIONS OF OCULAR TRAUMA Post - Traumatic corneal ulcers Any defect in the corneal epithelium may become infected Ulcers are surounded by a cloudy white or gray cornea Reactive sterile hypopyon may present in the anterior chamber Mx: opthamology consult, cycloplegics, topical abx, often admission (corneal perforation is a complication) Endophthalmitis Infection of deep structures of eye (anterior, posterior, vitreous chambers) Hx: pain and decreased acuity O/E: decreased acuity, chemois, hyperemia of conjunctiva, infected chambers (hazy or opaque) Complication of blunt globe rupture, penetrating trauma, FB, ocular surgery

Staph, strep, bacillus are common bugs Topical, intravitreal, systemic antibiotics are all used Sympathetic Ophthalmia Inflammation that occurs in the uninjured eye weeks to months after the initial insult thought to be an autoimmune response to the normally sequestered uvual tissues of the injured eye becoming exposed with the injury Hx: pain, photophobia, decreased acuity Tx: steroids, other immunosuppressants, optho consult, enucleation of blind eye can help

CONJUNCTIVITIS INTRODUCTION Conjunctivitis = Inflammation of the bulbar and palpebral conjunctiva Keratoconjunctivitis = Inflammation of cornea and conjunctiva Bacterial, viral, allergic, toxic, mechanical BACTERIAL Common bugs: Pnneumococcus, Hflu, Staph, Moraxella, Gonoccocus Uncommon bugs: Pseudomonas, Klebsiella Neonates: think of chlamydia and gonorrhea

Symptoms: irritation, FB sensation, lid swelling, drainage, eye crusting in morning NO photophobia or visual loss Cultures: only if Rx failure, severe infection, suspected gonorrhea, or neonatal Complications: corneal ulcer, keratitis, corneal perforation Treatment Warm compresses qid F/U in 5/7 if not improving (viral may last longer but bacterial usu doesn't) Topical antibiotics: fucopthalmic, polysporin ointment, or gentamycin 5-7d Avoid neomycin opthalmic solutions because of high incidence of hypersensitivity NO eyepatching NO corticosteroids If using topical antibiotics Ointments likely better b/c it stays longer; use polysporin bid Drops: use q2hr while awake, occlude lacrimal system after administration Neisseria gonorrhoeae Uncommon but important b/c of complications Direct contact from urethritis or pelvic infections Symptoms more severe; copious purulent drainage is a clue Gram stain may reveal diagnosis; cultures more sensitive (SEND cultures) Management more aggressive Mild: outpatient mx with ceftriaxone 1gm im, topical erythromycin ointment, saline irrigation, azithromycin 1gm po X 1 to cover concomitant chlamydia Moderate, Severe, any corneal involvement: admission, iv abx, saline irrigations, topical antibiotics Adults: cetriaxone iv, PCN 100,000 U/ml one gtt q2hr Neonatal: Manifests w/i 2 - 4 days after birth Look for sepsis (?LP, BC) Should do eye cultures Ddx: gonorrhea, chlamydia, HSV keratitis, dacrocytitis Tx: Pencillin 20,000 IU/ml ong gtt q1hr X 12hr Ceftriaxone 125 mg im X 1 Saline washes Add covererage for chlamydia

Chlamydia trachomatis Neonatal Manifests w/i 5 - 13 days after birth Topical erythromycin ointment, oral erythromycin X 14 days Chemical conjunctivitis from ointment administration immediately after birst occurs w/i 1 - 2 days

VIRAL CONJUNCTIVITIS

Bugs: adenovirus, coxsackie, entorviruses Hx: pink eye, drainage, more redness, more itching/irritation, periauricular lymphadenopathy, viral symptoms (rhinitis, cough, myalgias) Often starts in one eye then spreads to the other Management Artificial tears Cool compresses qid Can use topical antihistamine for itching (patanol) Epidemic KeratoConjunctivitis (EKC) Adenovirus Combined keratitis and conjunctivitis VERY CONTAGTIOUS Contagious for 10 - 12 days Average duration is 2 weeks but may last 4 weeks Often associated with a mild punctate keratitis by day 5-8 (80%); usually central; may be replaced by central subepithelial infiltrates which don't stain with fluroscence Characteristics Outbreaks of "pink-eye" Follicles on conjunctiva Thin pseudomembrane Management Cool compresses +/- antihistamines Wash hands thoroughly Examiner should wear gloves Slit lamp needs to be disinfected Avoid contact with family, throw out kleenex Stay home, out of day care for 2 weeks

ALLERGIC CONJUNCTIVITIS Drugs, cosmetics, environmental Itching is generally more pronounced : MUST be pruritic Stringy white discharge, itching, seasonal Symptoms tend to be bilateral (can be unilateral) May have chemosis (conjunctival edema) and/or blepharitis Vernal conjunctivitis Less common but more severe

Young males, hereditary, fhx of atopy Similar to allergic conjunctivitis but more itching The upper tarsal plate is "cobblestoned" from giant raised papilae which are pathognomonic for the disease (lower lid less common) Drainage is copious, thick, and ropy The cornea often has punctate lesions or can be ulcerated Tx: tears, cool compresses, cromolyn solution, aspirin, d/w optho Management Artificial tears: dilutes the allergen Saline eye drops help in 1/3 Cool compresses qid Patanol 0.1% one gtt bid X 7 days (topical antihistamine and mast cell stabilizer) Oral antihistamines may help TOXIC/CHEMICAL/ALLERGIC Toxic/chemical: exposures to irritants EYE DROP RELATED Common scenario: presents after being put on eye drops 5-7 days and things are getting worse instead of better; often multiple MD visits Many eye drops can irritate the eye and there can also be allergic reactions May have associated blepharitis R/O iritis etc Mx: stop all drops, cool compresses qid, f/u with optho likely warranted if going on that long BACTERIAL VIRAL ALLERGIC Copious purulent discharge Eye matted shut in am No hx Uni or bilateral Not generally pruritic No viral symptoms Less discharge volume and purulence No hx Bilateral > unilateral Prutitic Cough, rhinitis, fever, sore throat White, stringy discharge Hx of seasonal env allergies Almost always bilateral Very pruritic May have rhinitis

Bacterial vs viral Studies that look at eye cultures show we aren't very good at predicting who has bacterial vs viral conjunctivitis Abx necessary: Studies with culture proven bacterial infections were randomized to abx vs placebo and both resolved in ave 5 days (abx was slightly faster) UVEITIS/IRITIS Uveitis = inflammation of the iris (MC), ciliary bd, and choroid Iritis = inflammation of the iris (Acute, chronic, or recurrent) Associations/Etiologies Connective tissue disorders: RA, sjogrens, sarcoidosis, Behcet's Ankylosing spondylitis Reiter's syndrome Infections: TB, toxoplasmosis, toxocariasis, lyme dz, syphillus, leprosy

IBD Idiopathic Trauma Lymphoma Kawasaki's Symptoms Ocular pain/irritation Photophobia Blurred vision Signs Decreased VA Anterior chamber white cells: looks like floating dust particles Anterior chamber flare (protein): looks like headlights in fog Keratitic precipitates (spots on " back" of cornea) Hypophyon Perilimbal conjunctival injection: ciliary vessel hyperemia Posterior synechiae (remnant of prior iritis: pieces of iris stuck to the lens, can also occur with hyphemas) Management Oral analgesics Arrange optho f/u Discuss interim tx: steroids, cycloplegics EPISCLERITIS Inflammation of the tissue between the conjunctiva and sclera Common, benign, etiology unknown, often young adults FB sensation, irriation, photophobia, MILD pain Minimal tenderness Normal visual acuity Nodular localized pink/red conjunctiva and episclera Tx: artificial tears, optho prn SCLERITIS Vision threatening inflammation of the sclera Associated with CTD: young female with R.A. is the MC scenario Severe pain, wakes patient at night, "my eyes are killing me" Pain with EOM, DECREASED visual acuity, severe eye tenderness VERY red eye with prominent vessels that do NOT move when the overlying conjunctiva is moved with a cotton tip (clue to scleral inflammation) Associated uveitis and keratitis common Tx: consult optho, steroids, immunosuppressants DISEASES OF THE CORNEA PTERYGIUM/PINGUECULUM Pterygium

Wedge shaped area of conjunctival fibrovascular tissue that extends onto the cornea Pink, triangular, medial side is most common Benign proliferation of fibrovascular tissue May periodically become inflammed Refer to optho on a non-urgent basis (occasionally need excision) Pinguecula White, yellow, or brown flat to slightly raised tissue on the conjunctiva immediately next to but not on the cornea Looks like "heaped up" conjunctiva Near limbus on medial side is most common Amorphous conjunctival tissue adjacent to the limbus Periodically becomes inflammed Tx: protection from wind, dust, sunlight, and use artificial tears, topical NSAID if inflammed SUPERFICIAL PUNCTATE KERATITIS Superficial, punctate, multiple pinpoint corneal epithelial defects Nonspecific finding that is seen in many conditions Most common precipitant conditions are ultraviolet burns, conjunctivitis, topical eye drug toxicity (drugs with preservatives including artificial tears, gentamycin, neomycin), contact lenses, dry eye, exposure keratopathy, blepharitis, mild chemical injury, minor trauma, viral infections May present with pain, photophobia, redness, FB sensation Should consider HSV keratitis Minor Keratitis in non-contact wearer Treat associated condition Artificial tears (no preservatives) Topical antibiotics and/or cycloplegics Minor Keratitis Contact lens wearers Stop wearing contacts Ciprofloxacin opthalmic: 2 gtt q 15 min X 6hr, q30 min X 18hr WA, q1hr X 24hrs, q4hr X day 3 on

CORNEAL ULCERS AND INFILTRATES FROM INFECTION

Corneal infiltrates: focal white opacities without an epithelial defects Corneal ulcers: overlying corneal epithelial defect that stains with fluorescein in addition to the corneal infiltrate Contacts: pseudomonas and Acanthamoeba (swimming with contacts!) are common Usually starts as a minor corneal abraison which leads to bacterial entry Hx: pain, redness, irritation, photophobia, decreased acuity PE: decreased VA, conjunctival hyperemia, chemosis, epithelial corneal defect with dye uptake You can see anterior chamber cells, flare, hypopyon Tend to be central (further away from blood supply from limbus!) Corneal abraison vs ulcer MCC is bacterial, but fungal and HSV also occur Contact wearers: pseudomonas Managment: Discuss with optho D/C contact use Ciprofloxacin opthalmic HERPES SIMPLEX INFECTIONS Primary or reactivation Findings Punctate keratitis (early, first episode) Corneal dendritic ulcers: single or multiple (later, recurrent episodes); TERMINAL bulbs are pathognomonic for HSV ulcers Conjunctivitis Iritis Blepharitis: vesicles on eyelids History Pain, irritation FB sensation Blurry vision Exam Decreased visual acuity Conjuncitivits, keratitis, ulcer, uveitis, blepharitis Decreased acuity Tx Topical antiviral agents (trifluidine 1% q2hr X 2-3 weeks), topical prophylactic antibiotics and cycloplegics Acyclovir po if isolated eyelid vesicles NO topical steroids (contraindicated) Optho consult Neonatal: admit for iv acyclovir (usually associated encephalitis)

CONTACT LENS COMPLICATIONS List five complications of contact lens use Corneal abrasions Corneal neovascularization Keratitis Corneal ulcers (pseudomonas) Hypersensitivity reactions to solution (conjuncitivis, keratitis) Contact lens deposits Corneal ulcers due to pseudomonas a problem with contacts: corneal destruction in 24 hrs possible No s/s of infection: d/c contact lens use and f/u with opthamology Corneal infection suspected: optho consultation

HERPES ZOSTER Activation of virus along opthalmic division of trigeminal nerve leads to keratoconjunctivitis V1 Involvement: zoster at tip of nose (Huchinson's sign) is predictor of eye involvement in 75% due to involvement of nasociliary nerve (compared to 25% ocular involvement if V1 distribution does not involve tip of nose) Opthamology consult: various treatments with antivirals, steroids depending on location and severity Findings (many!) Punctate keratitis and pseudodendrites are the most common Pseudododentrites are formed from deposition of mucus, usually peripheral, and lack the rounded terminal bulbs at the end of the branches Corneal aneshtesia common Uveitis is 2nd most common finding Mild conjunctitivitis also common

STEROIDS + INFECTIVE KERATITIS = Scarring and possible permanent visual loss

PERIORBITAL CELLULITIS (Preseptal) Anterior to orbital septum Bugs: staph, strep, Hflu (kids) Strep is MCC Common in kids Abraisons, FB, sinusitis, and dental infections are common causes Physical - Periorbital cellulitic changes - Normal V.A. Clinical dx Mx Cefuroxime iv F/U with HPTP Admit if sick PO after 2/7

Swelling around the eyelid Red, warm around the eye History - NO pain with eye mvmt - Minimal pain - Normal E.O.M. - No proptosis - No eye pain with EOM

ORBITAL CELLULITIS

POSTERIOR to orbital septum Staph, strep, Hflu, anaerobes History Physical - Proptosis - Decreased V.A. Needs a CT orbits (look for gas, abscess) Mx Admit IV abx: clinda/gent Consult opthamology (may need I&D)

- Significant resting eye pain - Pain with ROM - Decreaed E.O.M. - Pain with E.O.M.

DISORDERS OF LIDS AND OCULAR SOFT TISSUES

HORDEOLUM (STYE)/CHALAZION Stye = External Hordolum Localized abscess of the meibomian glands in the eleylid near the root of the eyelash Essentially an eyelash abscess Presents with pain, swelling, redness, discharge Usually staph Difficult to distinguish from a chalazion Managment Warm compresses X 15 min, q2hr Many will decompress spontaneously Polysporin to conjunctival sac qid (decreases bacterial load to the area) Resolves in 7 days Oral abx if associated facial cellulitis Localized, nodular, inflammatory processes of the eyelids Surgery for chronic, failure of conservative rx Chalazion Chronic inflammation of meibomian glands and obstruction by fat an fibrious tissue that may result from a stye but is usually just obstruction of the gland Secretions are extruded into the tissue causing a local reaction Similar presentation Same management PEARL: older patient, recurrent/resistant: could be an eyelid tumore, refer DACRYOCYSTITIS Acute infection of the lacrimal sac from nasolacrimal duct obstruction Staph aureus is the MC organism, strep, Hflu Pain, tenderness, swelling, erythema over the lacrimal sac Pressure over the sac may express purulent material from the puncta Management Warm compresses q few hors Keflex or clavulin po Cefuroxime iv if severe/sick/immunocompromised (staph, strep, hflu) Refer if chronic or recurrent BLEPHARITIS Toxic, allergic, infection related Thick, mattered, red eyelid margins with pronounced blood vessles Burning, itching, tearing, FB sensation, morning crusting of eyelids Tx: rubbing the eyelid margins with a mild shampoo using a cotton-tipped applicator or cloth bid, warm compresses, artificial tears, topical antibiotic ointment if severe

GLAUCOMA PRINICPLES OF DISEASE Aqueous humor is produced by ciliary processes

Aqueous humor provides structural support to the anterior chamber, delivers oxygen and nutrients to the avascular lens and cornea and removes waste products Aqueous humor passes from the posterior chamber to the anterior chamber through the pupil Aqueous humor is transported into the trabecular meshwork located at the anterior chamber angle formed by the junction of the root of the iris and the peripheral cornea; the trabecular meshwork functions as a one-way valve and filter for the aqueous humor to drain into the canal of Schlemm which then drains into the episcleral veins Intraocular pressure (IOP): function of aqueous humor production/removal; N = 10 - 20 mmHg Glaucoma = optic neuropathy caused by increased IOP, irreversible damage can occur Classification Primary: NO associated ocular or nonocular event Secondary: associated ocular or nonocular event Closed angle: anterior chamber angle is narrowed reducing the outflow of aqueous humor Open angle: normal anterior chamber angle PRIMARY OPEN-ANGLE GLAUCOMA Most common form of glaucoma; a leading cause of blindness Increased resistance to aqueous humor outflow through the trabecular network Insidious onset, slowly progressive, chronic, bilateral, painless Advanced disease occurs before symptoms Hx: visual field loss that moves from periphery to central O/E: optic cup to nerve ratio > 0.6, vertically oval/deep/pale optic cup, nasal displacement vessels Tx: topical Beta - blockers, selective alpha2 agonists, carbonic anhydrase inhibitors, prostaglandin agonists, miotics, sympathomimetics -----------> argon laser trabeculoplasty ----------> guarded filtration surgery Topical medications CAN produce systemic side-effects: Beta-blockers have produced asthma, heart block, CHF, hypoglycemai Adrenergics have produced hypertension, arrythmias Carbonic anhydrase inhibitors: renal stones, hypokalemia Acetylcholinesterase inhibitors: prolonged apnea after succinylcholine SECONDARY OPEN-ANGLE GLAUCOMA Lens induced, inflammatory, exfoliative, pigmentary, steroid induced, traumatic, angle recession, ocular tumors Tx directed at underlying etiology and same meds as primary open-angel glaucoma SECONDARY ANGLE CLOSURE GLAUCOMA Pupillary block: may develop from swollen or dislocated lens, or posterior synechia (adhesions b/w the iris and lens) No pupillary block: secondary angle closure without pupillary block can be caused by intraocular tumors, CRVO, or postoperatively

PRIMARY ANGLE CLOSURE GLAUCOMA

Anatomic variation: occurs in patients who have anatomically small and shallow anterior chambers; results in iris being nearly in contact with the lens resulting in resistance to aqueous humor flow from the posterior to anterior chamber (pupillary block) Pathophysiology MAIN problem is the iris is "stuck to" the lens Iris bulges forward obliterating the angle between the cornea and iris obstructing the trabecular meshwork, decreasing outflow and leading to rapid rise in IOP Explains why the primary treatment is laster iridectomy (they aren't lasering the trabecular network) Precipitants = pupillary dilation Walk into dimly lit room Emotional upset Medications: anticholinergics, sympathomimetics Flat or plateau iris Less common mechanism Flat or plateau iris leads to a narrow angle recess Dilatation of the pupil causes the iris to fold and bunch over the angle blocking aqueous humor outflow Symptoms EVERY HEADACHE NEEDS THEIR EYES CHECKED: H/A + DILATED PUPIL HAS BEEN GLAUCOMA Eye pain Headache Blurry vision N/V Occassionally abdominal pain Halo around lights Signs Perilimbal conjunctival injection Conreal edema (steamy corneal appearance): fluid is forced into the cornea when IOP is > 50-60 range Mid to dilated pupil Sluggish reaction to light (or fixed) Decreased visual acuity Increased IOP (> 20, usually will be at least 40 and more like 70 range) General Management All require opthamology consult as definitive tx is surgical (peripheral iridectomy) Mild visual acuity loss and IOP < 50 ---------> topical medical management Significant visual loss (hand mvmts) and IOP > 50 ---------> topical and iv Rx Pharmacologic Approach Goals: decreased IOP by (i) miosis (ii) decreased aqueous humor production (iii) osmotic fluid shifts (iv) prevention of valsalva effects Timolol 0.5%: decreases aqueous humor production and decreases IOP in 30 min; also causes miosis Pilocarpine 1-2%: 1 ggt q 15 min X 2; cholinergic :. pupil constriction Apraclonidine 1%: A2 agonist Prednisolone 1%: q15 min X 4 Acetazolamide 250 - 500 mg iv: decreases aqueous humor production

Mannitol 1-2 mg/kg iv over 45 min: osmotic shift of fluid to decrease IOP Sedatives and Antiemetics: prevent agitation, N/V (valsalva -----> incr. IOP) T A P TIMOLOL 0.5 % gtt to other side Decreases acqueos humour production and constricts pupil. ACETAZOLAMIDE 250 - 500 mg iv or po Decreased acqeous humor production. PILOCARPINE 2% one gtt q 15 min X 2, one gtt to other side Repeat if pupil does not constrict. Causes pupillary constriction. ANALGESIA: morphine ANTIEMETICS: maxeran. MANNITOL 0.5 -1.0 gm/kg iv Osmotic shift to decrease IOP. Give early if pressures very high (>70) or if pressures don't respond to above within 30 min.

A M

PEARLS Space drops one minute apart Consult optho for mannitol recommendation, go ahead with the rest Treat first, phone later Check I.O.P. q 30 min: pressures should drop within 30 minutes

ANISOCORIA INTRODUCTION Head trauma or decreased LOC warrants immediate investigation/intervention Normal LOC is less concerning (head trauma, asymmetric pupils but normal LOC does not have significant intracranial pathology) Which pupil is abnormal? Pupil that has sluggish constriction is likely abnormal Anisocoria greater in the dark suggests the abnormal pupil is the smaller one Anisocoria greater in the light suggests the abnormal pupil is the larger one Anisocoria with normal afferent visual system: innervational or structural defect Structural defects usually detectable with slit lamp examination Normal slit-lamp exam, both react well to light ------> see whether anisocoria increases in light or darkness Anisocoria increases in light: adie tonic pupil, pharmacologic blockade, third-nerve palsy Anisocoria increases in dark: benign anisocoria, Horner's ADIE TONIC PUPIL Blurred near vision but normal distant vision Poor accomodation with a very slow constriction to near testing Pupil will redilate slowly when the vision is agoin mad distant Slit-lamp: sector palsies of the iris Young women, associated symmetrically reduced DTRs Diagnosis confirmed by weak cholinergic agent (pilocarpine 0.1%) causes intense pupillary constriction as a result of cholinergic supersensitivity in the affected pupil c/p to normal one Referral to optho on non-emergent basis for cholinergic therapy PHARMACOLOGIC MYDRIASIS Deliberate or inadvertant administration of sympathetics or parasympatholytic agents Sympathomimetics: phenylephrine or cocaine for nasal use may get into eye Paraympatholytics: atropine, scopolamine; transdermal scopolamine patches can cause anisocoria Pilocarpine 1.0% test: cholinergic agent that should constrict the pupil; will rapidly constrict the pupil if dilation is secondary to 3rd nerve palsy; will NOT constrict the pupil if due to anticholinergics THIRD NERVE PALSY Anisocoria, increases in light, no evidence of Adie tonic pupil or pharmacologic reason Almost always have other signs of 3rd nerve palsy: ptosis, EOM dysfunction Hx: diplopia O/E: pupil will be down and out (loss of sup rectus, medial rectus) MUST r/o aneurysm or other intracranial pathology

HORNER'S SYNDROME MIOSIS + PTOSIS + ANHYDROSIS Interruption of sympathetic innervation Dilation lag is classical finding: pupil requires up to 15 seconds to fully dilate Anisocoria will be greater at 3 - 5 seconds of darkness than 15 seconds although the anisocoria will still be more pronounced than in light Topical opthalmologic cocaine 10%: horner's pupil will dilate less than the normal pupil inreaction to cocaine Horner's etiology: CVA, CNS tumor, lung ca, thyroid maass, herpes zoster, OM, pancoast tumors, headache syndrome, carotid dissection, congenital horner's (birth trauma) Hydroxyamphetamine 1% administered 24hrs after the cocaine test can be used to determine the level of sympathetic interruption and dictate the work up New onset Horner's should have thorough work up PHYSIOLOGIC ANISOCORIA 20% of population has 0.4mm difference Transient, persistent, alternating pupils Increases in darkness, but NO lag seen as with Horner's

SUDDEN ATRAUMATIC VISUAL LOSS INTRODUCTION Usually monocular, duration seconds to days, vision generally 20/200 or worse Aggressive investigation to determine etiology Opthamomology or neurology consultation Acute visual loss may not be an acute process: sudden discovery of visual field loss Acute visual loss may not be related to eye Differential dx of sudden, atraumatic, painless, unilateral vision loss Spontaneous lens dislocation Vitreous hemorrhage Retinal detachment Central Retinal Artery Occlusion: embolism/TIA, vasculitis, sickle cell, migraine Central or Branch Retinal Vein Occlusion Ischemic Optic neuritis: TIA, migraine (should have pain), vasculitis, sickle cell Inflammatory optic neuritis (usually painful) Conversion disorder CHIASM OR BEHIND WOULD BE BILATERAL Malingering Differential dx of sudden unilateral PAINFUL blindness Acute angle closure glaucoma Inflammatory optic neuritis Differential dx of bilateral visual loss Bilateral ischemic optic neuritis Bilateral inflamatory optic neuritis Optic chiasmal lesion: tumor, craniopharyngioma, meningioma (bitemporal hemianopsia) Optic radiation: infarct, bleed, tumor, abscess, trauma (homonomous hemianopsia or quadrantaopia) Optic cortex: infarct, bleed, tumor, abscess, trauma (homonomous hemianopsia) Conversion Malingering Differential dx of complete bilateral visual loss Conversion Malingering Any of the above but bilateral (unusual) Large chiasmal event Papilledema POSTERIOR VITREOUS DETACHMENT Very common > 60 yo Vitreous gel pulls away from the retina with aging which can lead to symptoms similar to retinal breaks, vitreous hemorrhage, and retinal detachment No specific treatment is indicated unless accompanied by a retinal break, vitreous hemorrhage, or retinal detachment

Should have prompt evaluation by opthamologist to r/o associated retinal pathology

VITREOUS HEMORRHAGE Definition = bleeding into the preretinal space or int the vitreous cavity Etiology Retinal tears and detachment are the MCC Diabetic retinopathy Trauma Intraocular tumors Retinal microaneurysms Vitreous detachment Sickle cell dz Macular degeneration of the retina History Floaters = Cobwebs in vision = Snakes/spiders in vision Flashers if associated retinal tear Blurry vision Signs Decreased red reflex (may be absent or black) Reddish haze of vitreous Worms Decreased visual acuity Retinal detachment might be seen Afferent pupillary deficit might be seen (retinal detachment) Long-standing preretinal hemorrhages can become a whit mass that may look like tumor/infection Managment Consult optho Bed rest, elevation of head, no anticoagulants or antiplatelet agents Definitive tx targeted at underlying cause Vascular retinopathy: laser photocoaguation or cryotherapy Retinal tears or detachments: repaired U/S to determine if retinal detachment is present and may determine the cause Vitrectomy in certain cases

RETINAL BREAKS AND DETACHMENT Retinal layers: inner neuronal retina, outer pigment epithelial layer Layers can be separated by fluid Retinal break is a tear in the retinal membranes and may or may not lead to retinal detachments Retinal detachments occur by three mechanisms: exudative, tractional, rhegmatogenous Rhegmatogenous Tear/hole in neuronal layer (vitreous fluid leaks b/w and separate the two layers) Generally >45yo, more common in men, associated with degenerative myopia Trauma may be associated with rhegmatogenous detachment by causing tears in the retina or disinsertion of the retina from its attachment at ora serrata anteriorly Traumatic retinal detachments can occur at any age; increased risk with myopia Exudative Result of fluid or blood leakage from vessels within the retina Hypertension, toxemia of pregnancy, CRVO, glomerulonephritis, papilledema, vasculitis, choroidal tumor Traction Consequence of fibrous band formation in the vitreous and band contraction Fibrous bands result from the organization of inflammatory exudates or blood from prior vitreous hemorrhage History Flashers: traction and stimulation of retina Blurry vision (described as filmy, cloudy, curtainlike appearance) Floaters if associated vitreous hemorhage Absence of pain Signs Decreased visual acuity (can be minimally changed) Visual loss is commonly Visual field loss relates to location and size Afferent pupillary defect only if detachment is large Detachment visualized via opthalmoscopy: retina will appear out of focus; bullous detachment with retinal folds are seen with large detachments Indirect opthalmoscopy is needed to r/o detachment b/c direct fundoscopy cannot visualize the anterior portions of the retina Management Difficult to see, refer based on history Macula involved is more urgent Some forms require urgent surgical repair Acute retinal breaks are surgically repaired w/i 24hrs

All other acute rhegmatogenous and tractional retinal detachments can be repaired w/i a few days Exudative detachment: tx underlying cause, laser photocoagulation Suspected retinal break or detachment requires emergent optho consult

BRANCH (BRVO) and CENTRAL RETINAL VEIN OCCLUSION (CRVO) Painless loss of vision due to CRVO causing edema, hemorrhage, vascular leakage Wide spectrum of appearances and depends on degree of venous obstruction Minimal loss of vision to near total loss of vision Associations: CVD, HTN, DM, OCP, > 50yo, vascultits History = blurry vision Nonischemic findings Minimal fundus changes NO afferent pupillary defect Visual loss minor (2/3 of pts having 20/40 or better) Retinal hemorrhages Ischemic findings: Marked abnormal fundus = blood and thunder Blurry disc margin Dilated, tortous veins Cotton wool spots Retinal edema Marked decreased visual acuity Often an afferent pupillary defect Branch retinal vein occlusion Distal to an AV crossing and hemorrhages occur distal to the site of occlusion Symptoms depend on location; often asymptomatic if macula spared Retinal edeam, superficial hemorrhage, dilated vein Mx: nothing or photocoagulation depending on location/severity Neovascular glaucoma is major complication of ischemic CRVO Emergent optho consult Treatment: complex, decreasing IOP, steroids, cyclocryotherapy, photocoagulation CENTRAL RETINAL ARTERY OCCULSION (CRAO) Painless acute visual loss due to occlusion of central retinal artery Painless sudden loss, r/o lens dislocation, vitreous hemorrage, retinal detachment Occlusion causes an ischemic stroke of the retina 50 - 70 yo, 50% have carotid atherosclerosis RF: HTN, CV dz, DM, collagen vascular dz, vasculitis, valve disease, sickle cell dz, increased intraocular pressure (glaucoma, retrobubar hemorrhage, endocrine exopthalmos) 100 minutes until complete visual LOSS

Hx: sudden visual loss over seconds O/E: markedly reduced visual acuity, prominent afferent pupillary defect Edematous retina with pale gray-white appearance and the fovea appears as a cherry-red spot Management Digital Global Massage: begin immediately, apply direct digital pressure through closed eyelid for 15 seconds then sudden release Breath in a bag: Increased PC02 to retinal artery to cause vasodilation: rebreathing into a bag for 10 min each hour Consult optho stat: ? LYTICS, anterior chamber paracentesis, mannitol etc Reduce IOP; timolol 0.5% topically, acetazolamide 500mg iv or po will lower IOP and retinal blood flow increases NEUROOPHTHALMOLOGIC VISUAL LOSS Visual loss not explained by physical examination Decreased vision and decreased visual acuity VS Visual loss but have normal visual acuity (careful visual field testing important)

PRECHIASMAL VISUAL LOSS Decreased visual acuity or visual field loss in the eye on the affected side May be unilateral or bilateral Affected side will have afferent pupillary defect unless the process is bilateral (may be a relative afferent defect) Visual field defects do not respect the vertical meridean and is often localized to the center of the visual field Etiology: optic neuritis, ischemic optic neuritis, compressive optic neuritis, toxic and metabolic optic neuritis Optic Neuritis Acute monocular loss of vision caused by demyelination of the optic nerve Age usually 15 - 40 Hx: visual loss over hours to days, ocular pain with eye mvmt O/E: acuity can be minimal loss to near blindness; afferent pupillary defect always present, central scotoma is MC visual field defect Fundoscopy: normal or swollen disc Nhx: visual acuity reaches its poorest w/i 1 week, then slow improvement over the next few weeks; 30% will develop MS in next 5years Methylprednisolone IV X 3/7 versus po prednisone vs no steroids: controversial, may speed recovery but NO effect on long-term vision or rates of MS Ischemic Optic Neuropathy (ION) MCC of optic neuropathy and is one of the MCC of visual loss past middle age Temporal arteritis

giant cell arteritis weight loss, malaise, jaw pain, headache, scalp tenderness, PMR, low grade fever, severe painless visual loss extremely rare < 50yo visual loss can be sudden, severe and bilateral study: unilateral 50%, sequential 35%, bilateral 15% occassionally preceded by amaurosis fugax large afferent pupillary defect, visual field defect may respect the horizontal meridian optic disc is pale and swollen ESR: men (age/2) vs women (age+10/2) temporal artery biopsy for definitive dx start steriods ASAP; ie, before biopsy, ESR methylprednisolone iv > prednisone po (less visual loss)

Non-arteritic Ischemic Optic Neuropathy much more common than temporal arteritis lack classic symptoms of temporal arteritis and have normal ESR vasopaths: DM, smoking, HTN, cholesterol, etc temporary, followed by headache ------> migraine with vasoconstrictive phase leading to amarosis fugax painless visual loss, afferent pupillary defects, disc swelling, visual field defects that respect the horizontal meridian visual loss more severe than temporal arteritis improvement in 1/3 steroids controversial: tx with steroids while waiting bx if there is any chance that it may be temporal arteritis Compressive Optic Neuropathy Tumor, aneurysm, sphenoid sinusitis or mucocele, blunt trauma, thryoid disorders Often involves chiasm Visual loss that continues to progress over 7 days Tends to involve other cranial nerves (helps distinguish b/w optic neuritis) Head CT or MR to r/o compressive lesion (consider if presentation is atypical for optic neuritis or ischemic optic neuropathy) Toxic and Metabolic Optic Neuropathy Bilateral, symmetric, can be severe, visual field defects are central Toxins: methanol, ethylene glycol, barbiturates, chloramphenicol, emetine, ethambutol, isoniazid, heavy metals Metabolic: thiamine deficiency, pernicous anemia Treatment based on cause

CHIASMAL VISUAL LOSS Chiasmal compression by pituitary tumors, craniopharyngioma, or meningoma Gradual and progressive visual loss

Classic defect is bitemporal hemianopsia BUT optic nerve compression often also occurs and leads to combinecd central and temporal visual field loss Any time the visual field defect respects the vertical meridian from a neuroophthalmic loss, the lesion is out of the globe and must be chiasmal or postchiasmal POSTCHIASMAL MCC are infarction, hemorrhage, tumor, AV malformation, migraines Optic tract ------------> visual cortex (occipital cortex) Classic defect is homonomous hemianopsia Cortical blindness: caused by bilateral occipital infarctions, often mistaken for functional blindness b/c NORMAL fundoscopy and NORMAL pupillary reflexes Anton's syndrome: bilateral blindness, normal pupillary reflexes, bilateral occipital lesions, and DENIAL of blindness

FUNCTIONAL VISUAL LOSS Conversion reactions (hysteria) and Malingering Conversion reaction: pt unaware of absence of medical problem and is not motivated by secondary gain; flat affect under circumstances of visual loss (should be freaked out!) Malingerer: aware of absence of pathology, motivated by secondary gain; usually dramatically emotional Clues: NORMAL fundoscopy, NO afferent pupillary defect, NORMAL pupillary reflexes Tests to TRICK Hesitant to try to oppose index fingers of each hand Write name in disorderly fashion (blind can usually write w/o problems) Mirror in front of face, ask patient to look straight ahead, tilt mirror slightly back and forth ------> MOST will follow their reflection in the mirror as it changes position proving feigned visual loss

MACULAR DISORDERS Many disorders affecting macula can cause acute visual loss Key to dx: loss of central vision with preservation of peripheral vision C/o central visual disotrostion and anatomic changes Vascular, infections, trauma, inflammatory, toxic, radiation, hereditory, idiopathic Infection/Inflammation Bacterial, viral, protozoans can cause maculopathy

Inflammaotry debris from exudate may fill the vitreous leading to a cloudy appearance Severe pain, redeness, periocular edema common Lesion will appear white if the retina and choroid are obliterated Emergent optho consult Age - related macular degeneration Most common reason for visual loss >65yo; usually gradual onset but can be rapid Drusen: small sharply defined yellow-white masses Some develop a choroidal (preretinal) neovascular membrane which appears as a grayish-green membrane beneath the retina --------> can lead to hemorraghe, transudation, scar fromation, or exudative detatchment of the retina Large hemorhage form the neovascular membrane can cause severe visual loss and may break through the retina into the vitreous causing peripheral loss Laser photocoagulation is the tx for choroidal neovascular membrane and should be done as soon as possible

MISCELLANEOUS OPTHAMOLOGY PAPILLEDEMA Changes in optic disc from increased intracranial pressure Etiology: blood, tumor, pus, CSF (pseudotumor cerebri) Swelling of optic disc and blurring of disc margins, hyperemia, and loss of physiologic cuppin Flame-shaped hemorrhages and yellow exudates appear near the disc margins as the edema progreses May be asymptomatic; symptoms variable and depend on etiology Visual acuity NOT affected until papilledema longstanding Brief obscurations of vision, enlargement of blind spot, inferior nasal field loss are common Bilateral process but may be asymmetric Mimics of pepilledema: CRVO, papillitis, hypertensive retinopathy, ischemic optic neuropathy, optic disc vasculitis, diabetic papilliits with retinopathy Required CT head NYSTAGMUS Clinically significant nystagmus is an oscillation of the eyes that occurs w/i 30 degrees of the midline Pendular nystagmus is of equal velocity in both directions Jerk nystagmus has velocity greater in one direction Pathologic movement is the SLOW movement; cortex is the compensatory FAST movement Monocular or binocular Conjugate (both eyes moving in same direction) or disconjugate (eyes moving in opposite directions) Primary gase position or gaze positi8on Congenital nystagmus Birth or neonatal period

Horizontal, conjugate, bilateral, symmetric and peduncular May become jerky on lateral gaze but remains horizontal despite upward or downward gaze Damped by convergence, increased with fixation, accentuated by covering one eye, and abolished with sleep No neurologic complaints Acquired nystagmus Toxic, retinal, labyrinth, vestibular nuclei, BS lesion, CB lesion

DISORDERS OF OCULAR MOVEMENT Diplopia caused by certain eye movements: monocular or binocular? Monocular: less concerning, usually refractive errors, dislocated lens, iridodialysis, feigned disease Binocular: disappears with either eye covered Mechanical: hematoma, orbital floor fracture, abscess Muscular: hypothryoid, muscle fibrosis NMJ: myasthenia gravis (PD3) CN palsies: III, IV, VI BS (CN nuclei): multiple sclerosis, CVA, etc Third Nerve Palsy Fourth Nerve Palsy Easily missed Superior oblique paresis (LR6SO4) Diplopia made worse by downgase, gaze away from paretic side Head tilt to the opposite shoulder to compensate for the vertical extorsion and will have weakness in downward gaze Trauma, vasculare, aneurysm, tumor, myasenia gravis Sixth Nerve Palsy Esotopia that is worsened by lateral gaze and will often turn their heads laterally toward the paretic side to compensate Aneurysm, vascular disease (DM, HTN, AS), trauma, tumor, MS, meningitis, thyroid eye disease, any cause of increased intracranial pressure (false localizing sign) OPHTHALMIC MEDICATIONS Drops increase concentration in eye, reduces unwanted side-effects, rapid absorption, brief effect, minimal interference with visual media but are rapidly cleared by tears

Multiple eye drops: should wait 10 minutes b/w drops Digital pressure to medial canthus prevents drainage vial nasolacrimal duct Remember that systemic absorption can cause side-effects (BB and asthma) Topical anesthetics: aid examination, never prescribe Antibiotics and antivirals: guided by suspected organism Corticosteroids: commonly used by opthamologists, minimal role in ED; post - traumatic iridocyclitis is probably only situation for ED used NSAIDs: topical use good for a variety of inflammatory conditions Artificial tears Cycloplegics Block muscarinic receptors of ciliary muscle; always cause mydriasis Relief of pain from ciliary spasm related to corneal abrasions, ocular truama, and iridocyclitis Mydriatics dilate the pupil but not all mydriatics are cycloplegics Mydriateics contraindicated in hx of glaucoma, increased IOP, shallow anterior chamber, suspected globe rupture, lens inplant present Atropine: long duration of action (weeks) and best avoided in ED

RED EYE Conjunctivitis (inflammation of conjunctiva): bacterial, viral, allergic, toxic Bacterial, viral, allergic, toxic Episcleritis (inflammation of tissue b/w the conjunctiva and sclera) Vascular dilation or edema, nodular (CVD, gout, RA, zoster) Scleritis (inflammation of sclera) Keratitis (inflammation of cornea) Bacterial, viral, fungal Zoster Iritis (inflammation of iris)/Uveitis (inflammation of uveal tract - iris, ciliary body, choroid) Sarcoid, ankylosis spondylitis, TB, reiter's, toxoplasmosis, toxocariasis, jeuvenile RA, lyme dz, IBD Acute angle closure glaucoma

NEUROPTHAMOLOGY 1. VISION (a) visual acuity = resolving power, spatial limit of visual discrimination, ability to make out detail - requires accurately focussing lens, fovea, pathway to occipital cortex - neither the entire retina nor the visual pathway need to be completely normal to have visual acuity - measured by snell chart - Pt at 20 feet - 20/40 means from 20' Pt sees what a normal person could see from 40 feet - 5/400 means from 5' Pt sees what normal person sees from 400' - snell chart finger count hand mvmt penlight no light perception - bedside: use glasses, 14" (b) visual field = visual space where objects are simultaneously visible while fixating on a target - check by confrontation - image is inverted and reversed on the retina (nasal field temporal retina, etc) - review visual pathway - constant retinotopic distribution o f fibers in the pathway - lesions in and behind the chiasm produce defects in both eyes

(C) color perception (d) contrast sensitivity - it measures the way we really see thing as contrasts of form and shape and not as black letters on a white background which represents 100 percent of contrast - optic neuritis ­ may recover acuity but not contrast sensitivity thus they complain of the view being "washed out" - greatest contrast sensitivity b/w 3-5 cycles per degree of arc 2. OCULAR MOTILITY - binocular single vision (BSV) provides stereopsis which is the ability to view the env. In three dimensions - initiation of gaze mvmts - frontal eye field of frontal lobe supranuclear pathways CN 3,4,6 nuclei - parietal-occipital lobes also contribute - EOM - MR = ADduction - LR = ABduction - SR = elevation and ABduction - IR = depression and ABuction - SO = depression and ADuction - IO = elevation and ADduction 3. PUPILLARY FUNCTION (a) light reflex pathway (b) ocular sympathetic pathway - stimulus = load noise, fear - hypothalamus ­ BS ­ T1 SC ­ paravertebral symp chain (second order) ­ synapse In the superior cervical ganglion ­ postgangl fibers (third order) run w ICA ­ enter orbit ­ dilator of pupil

(c) near reflex and accomodation - near synkinesis = convergence + accomodation + miosis (constriction) with conscious visual effort at a near object (d) anisocoria = unequal pupils - never due to optic n. disease b/c of dual crossover and always implies an efferent defect of either the occulomotor n. or sympathetic paresis THE NEUROPTHAMOLOGICAL PATIENT - problems are afferent visual symptoms or s/s of ocular motility disorders 1. Afferent System Disorders - history - visual loss Hx, one or both eyes, onset and progression, duration, pain, past Hx? - examination - the most important test is the pinhole test - visual acuity improves refractory error or media disturbance (cornea, lens, etc) - visual acuity does not improve - exclude a large media opacity (appear black w red reflex) - visual loss or optic nerve disease? Do a swinging flashlight test 1. shine in good eye and see direct and consenual response 2. Shine in poorer eye 3. Shine in good eye again (keep there for 5sec until stabile) 4. Rapidly swing the light across the nose bridge - if poor eye constricts and then returns to the previously stabile size the vision loss is solely retinal in origin - if poor eye dilates instead of constricts the visual loss is due to optic nerve disease - opthalmoscpe exam also helps (atropy vs macular deg 2. DISORDERS OF OCULAR MOTILITY - less than 10 - usu present with strabissimus - require full opthamological exam b/c dev'p into amblyopia - adults - usu present with diplopia - note: monocular diplopia is possible - small opacities, lens hardening can cause it - usu reported as "ghosting" - pinhole relieves the diplopia and makes the Dx - binocular diplopia - horizontal or vertically displaced?\ - maximal displacement in what direction? - onset acute or chronic, constant or intermittent - pain, headache - worse at near or far - examination - look for ptosis, dilated pupil in examination - forced duction test (FDT)

= attempt to move the eyeball in the direction of the paralyzed muscle - if you cannot move the eyeball it implies that there is restriction by the antagonistic muscle - seen in Grave's disease (MR restriction thus you cannot abduct) - exclude.... - MG by tensilon test - decompensated latent strabismus - deviation is constant and full EOMs

GLAUCOMA ** affects 2% of population ** key to prevention is early Dx and Tx, it can be controlled but not cured = group of diseases characterized by an IOP of sufficient degree to cause optic nerve damage and visual field changes - not all have high IOP - normal IOP = 10-21mmHg w/ ave = 17mmHg - normal (low) tension glaucoma = optic nerve change is consistent with glaucomatous neuropathy and visual field changes are found in a Pt that has never had an IOP > 21 - occular HTN = IOP is contiually > 21 but has a normal optic nerve head and visual fields - optic nerve and cup to disc ratio - normal cup:disc ratio is 0.3 - 0.3 - 0.7 should be investigated - >0.2 assymetry b/w eyes should be investigated - progressive enlargement of ratio is an indicator

- can lose up to 50% b/f any visual field loss detectable - visual field - sharp vision preservation = glaucoma commonly causes loss of the peripheral preservation of the central field - thus, often present late with significant damage - risk factors - IOP - positive family Hx - age - diabetes - HTN - race (B>W) - screening - most Pts are asymptomatic at time of diagnosis - IOP is a poor indicator alone - best screen for glaucoma is the optic nerve head

field with

OPEN ANGLE GLAUCOMA: -Primary open angle glaucoma = IOP > 21 w/ optic nerve damage and visual field changes, usu bilateral - Normal (low) tension glaucoma = IOP <21 but w/ optic n. damage and visual field change - Ocular hypertensives = IOP > 21 w/ no problems - incidence = 60% - pathology - drainage doesn't work thus inc IOP - treatment - FIRST LINE - beta-blockers (topical) - do not use in heart block or COPD - SECOND LINE - adrenalin (propine is a prodrug) - s/es = stinging, headache, allergic conjunctivitis - pilocarpine (mitotic) - s/es = difficult night vision, myopia, headache (ciliary bd spasm) -THIRD LINE - carbonic anhydrase inhibitors (diamox) - dec IOP by 50% - limited use b/c of s/es ­ malaise symptom complex, GI symptom complex, Renal calculi, stevens-Johnson syndrome, blood dyscrasias -FOURTH LINE - argon laser trabeculoplasty - used w/ uncontrolle IOP on full meds - burns the trabecular meshwork to inc drainage -SURGERY - last resort, makes a new drainage CLOSED ANGLE GLAUCOMA: - 12% = Due to mechanical obstruction by the peripheral iris - F>M, 1in 1000 after 40yo

- precipitated by mydriasis (watching TV in dark room) - presentation - periocular pain + rapid, progressive vision loss + eye congestion + N + V - halos around the eye are due to corneal edema - Tx 1. Miotics - constrict the pupil and pull iris away from angle 2. Diamox - dec the IOP 3. Hyperosmotic agents - dec IOP by drawing water out of eye - oral glycerol, iv mannitol (better), 4. Laser iridotomy - definitive Tx, done to both eyes b/c other eye has 50% chance of developing CA glaucoma as well CONGENITAL GLAUCOMA: - 3% - autosomal recessive w/ incomplete penetrance, 1/10,000 births - 70% bilateral - signs - classic triad = tearing + photophobia + blepharospasm - corneal edema, enlargement, and clouding - Haab's striate = tears in descemet's mem - treatment - surgery is preffered - topical drops and po CA-Is used until surgery - prognosis - better if they present in first 1-24 mnths - more difficult to ctrl if present at birth or w/i first month

SCREENING = OPTIC NERVE HEAD + IOP MEASURE IOP IN THOSE > 55yo IN ROUTINE PHYSICAL

RETINAL DETACHMENT = separation of neurosensory retina from the underlying retinal pigment epithelium resulting in the loss of oxygen supply to the outer retina which is dependent of diffusio the choriod visual loss

from

CLASSIFICATION: 1. rhegmatogenous = spontaneous detachment secondary to a retinal tear/break 2. Tractional = any process putting traction on the retina (fibrous tissue in PDR, or penetrating trauma) may separate the retinal from the RPE 3. Exudative = tumor, inflam, etc. results in fluid accumulation POSTERIOR VITREOUS DETACHMENT:

= separation of the vitreous from the retina: increases with age b/c the hyaluronic acid In the vitreous decreases w/ age :. collagen fibrils shift and small pockets of liquid vitreous develop and eventually gain access to the space b/w the vitreous and the retina - most rhegmatogenous detachments are preceded by a PVD - vitreous base = firm vitreous attachment of collagen fibers to the retina and pars plana at each side of the ora serrata SYMPTOMS OF PVD: 1. Photopsia = sensation of flashing lights due to mechanical traction on retina 2. Floaters = black spots or wavy lines in the visual field due to vitreous aggregates, avulsed epipapillary glial tissue, or limited vitreous hemorrhage 3. Blurred vision = due to a shower of floaters or diffuse vitreous hemorrhage Vitreous hemorrhage results from a break or avulsion of a retinal bv as the PVD occurs. - significance of symptomatic PVD - 15% have a retinal tear - must be referred imediately for dilated fundic exam - may be possible to Tx w/ laser photocoagulation or externalcryotherapy which will usu prevent retinal detachment CONDITIONS PREDISPOSING TO RETINAL DETACHMENT: - occurs spontaneously, w/o trauma in 10/100,000 per year - associated conditions 1. myopia ­ more PVDs, more lattice degeneration, thined retina b/c of inc length 2. aphakia/pseudophakia ­ cataract extraction - general popn rate of retinal detachemnt = .05% - phacoemulsification or extracapsular extraction = 0-2% develop RD - intracapsular extraction = 2-5% develop retinal detachment 3. Trauma ­ blunt trauma is the leading cause in children 4. Lattice degeneration ­ inner retinal degeneration :. retinal thinning that shows a lattice resulting in retinal holes and tears; direct cause of 21% of Rds, More common in myopics 5. Other ­ inflam, degen, ....

SYMPTOMS OF RETINAL DETACHMENT: 1. Symptoms of PVDs ­ flashers + floaters + blurred vision 2. Visual field loss ­ peripheral scotoma (shadow) that is constant in location, of constant increasing size, that enlarges from the periphery toward fixation, and extends to the peripheral extent of the visual field ­ cannot see around it 3. Unilaterl blurred vision **URGENT REFERRAL - outer retinal layers have lost their direct O2 supply - inner retinal layers retain supply from the central retinal aa.

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