EyeBalls on Parade Lecture 1 - Essentials of Anatomy & Physiology -3 leading causes of blindness in US are: 1)DM, 2)Glaucoma, and 3)Macular

degeneration -CN VII closes eye (orbicularis oculi), III opens eye (levator palpebrae) -Levator Palpebrae + Muellers muscle/Superior Tarsal (sympathetic) opens eyelid -Orbicularis closes eye Canal/Fissure Structures running through Optic nerve + meningeal sleeve Optic Canal Ophthalmic artery + sympathetic complex Lacrimal nerve Superior Orbital Fissure Frontal nerve Superior Ophthalmic Vein Trochlear nerve Oculomotor nerve Nasociliary nerve Abducent nerve Maxillary nerve Inferior Orbital Fissure Infraorbital nerve Zygomatic nerve Pterygopalatine ganglion branches Inferior ophthalmic vein -Orbital fracture usually in lamina papyracea (orbital floor) -When injured, Endothelium does NOT proliferate --- Epithelium does -Cataract is a normal aging process; just thickening of the lens with age -Scotoma = reduced/absent vision; blind spot; may look like a cracked mirror or heat off pavement to the pt -Hemianopia = loss of visual field -Homonymous = loss of right or left visual field -Lesions! -Anterior to chiasm = monocular loss -Chiasmal = bitemporal hemianopia -Posterior to chiasm = homonymous hemianopia -Cupping is out-pouching of optic disc -Macula --- 1:1 rods to cones, avascular; where fine vision is from -Metabolism is very important for transparency, mainly in lens epithelium -Anaerobic glycolysis, TCA, Hexose monophosphate shunt, and Sorbitol pathway; utilizes every type of metabolism weve learned about! -Glucose enters through the aqueous humor and is rapidly metabolized -Sorbitol Pathway: Usually only 5% of glucose metabolism, but with hyperglycemia (DM), it gets shunted down this pathway utilizing Aldose Reductase -Lens swells and blurs visioncataracts -Sorbitol CANNOT diffuse out of lensosmotic influx of H20 = edema, separation of lens fibers, loss of transparency, refractive changes. Chronically this process leads to cell lysis w/release of cellular contents and early cataract development. -Sorbitol Fructose (CAN diffuse out of lens) but takes 6 weeks for vision to go back to normal -Reactive surface of eye = Cornea (2/3) and Lens (1/3)if different, then Astigmatism; cornea = point and shoot lens = focus -Astigmatism uneven curvature of the cornea; causes separate areas of focus and consequent blurring -Accommodation = ability of ciliary muscle to contract for lens to focus; look near, pupils will constrict and eyes converge -Hyperopia = Farsightedaxial length short you can see far; images focus behind the retina -Myopia = Nearsightedaxial length long you can see near; images focus in front of the retina -Presbyopia = loss of accommodation (focusing) w/ age (early 40s)CANNOT be halted w/ refractive surgery -Photophobia = Iritis until proven otherwise -Visual Acuity = best corrected monocular vision (distance, near, color, Amsler grid) -20/200 = Legal Blindness -Corrective Surgery: See notepool if you really want to

Lecture 2 -The Ocular Exam -Visual Acuity 1st (except in chemical burns) -Best corrected monocular vision Distance (Snellen), Near (Rosenbaum) -Color with pseudochromatic plates - red/blue/greendefect usually x-linked but can be acquired d/t drugs or O.N. damage -Amsler Grid - testing macula for scotoma/metamorphopsia10 degrees from fixation of central vision -Visual Fields Confrontation; check for scotomas and any other visual defects/lesions -External Exam lids, eyebrows, eyelids, eyelashes, lacrimal glands, lymph nodes, proptosis/exophthalmos -Top 3 Complaints Seen in Ophthalmology: 1) Disturbance of vision diplopia, reading problems, blurred vision, color changes, etc. -**anytime you hear floaters and photopsia (flashes of light) you MUST think retinal detachment** 2) Pain or discomfort in/about eyes foreign body sensation, burning, headaches, etc. -Itching = allergies; photophobia = iritis 3) Abnormal eye secretions -Purulent bacterial - Mucus allergy -Serous - viral -Cornea: Cornea Sensitivity = CN V -Fluroescein Staining of Corneadetects epithelial defects (visualize w/ cobalt blue filter) -Corneal abrasions are VERY painful (worse than childbirth?) -Arcus Cornea corneal degeneration which could be d/t dyslipidemia -Anterior Chamber Assessment of Depth with Side Penlight Test normal = deep; if shallow think glaucoma -Refer cataracts when decreased vision interferes w/ ADLs (patient decides if they need surgery, not physician) -Pupillary Testing: DO NOT USE PERRLA!! -Direct size (mm), equal, anisocoria (unequal size of pupils), reactive to light -Consensual -Swinging - detects afferent reflex (II in / III out); most important; RAPD = Relative Afferent Pupillary Defect -Pupillary Defects: -CN III defect dilated pupil (pupil sparing), EOM paresis/palsy (eye will be aBducted), ptosis -Adies Tonic Pupil = usually post-viral syndrome involving ciliary ganglion leading to blurred vision (esp. near), periocular discomfort, and decreased depth perception. D/t pupil that barely moves and is not completely round -Pharmacologic Pupil = often medical personnel or medications; allergy, cold, or motion sickness -Horners Syndrome = SNS pathway lesion leading to: Ptosis, Miosis, Anhydrosis (lack of sweating) -Argyll Robertson Pupil (Prostitutes Pupil ) = pupils accommodate but do not react to light, are irregular and small. Associated w/DM, EtOH, and Syphilis -Cover-Uncover test checking for strabismus; best for checking EOM alignment -EOM tests especially when c/o of diplopia Right + Up Lest + Up -Right superior rectus -Left superior rectus -Left inferior oblique -Right inferior obliquee Right Left -Right lateral rectus -Left lateral rectus -Left medial rectus -Right medial rectus Right and Down Left and Down -Right inferior rectus -Left inferior rectus -Left superior oblique -Right superior oblique -Opthalmoscopy red reflex, cup:disc ratio, circulation, macula, etc. -Nystagmus spontaneous back-and-forth movement of the eye(s); can be d/t drugs, CNS lesions, physiologic, tumors, etc. -Common causes of diplopia = III/IV/VI Palsy, Myasthenia Gravis, Graves, Blowout fracture -Do NOT dilate if shallow chamber, neurological pt, iris supported lens -Schiotz Tonometrynormal 10P 10-21 mmHg, anesthetize w/ proparacaine, separate lids w/out pressure -Record and convert to IOP -***Eye Exam Steps Summary (KNOW THIS!!)*** -Measure best corrected monocular VA, Perform VF via confrontation, Inspect external (lid, lashes, lymph nodes), Inspect conjunctiva & sclera, Test EOM, Pupillary testing, Inspect cornea & iris, Assess A/C depth, Assess lens clarity, Fundus exam (C/D, A/V, macula), Perform tonometry if indicated -Refer if*** -VA <20/20 if visual complaints -VA <20/40 even in absence of complaints -VA asymmetry --- difference of 2 lines or more -Fundus abnormality -Shallow A/C or IOP > 22 mmHg

Lecture 3 - Acute Visual Loss I -Disease Etiologies: PD VITAMIN C (Psychiatric/functional, Drugs, Vascular, Infectious, Trauma, Autoimmune/Allergy, Metabolic, Idiopathic/Iatrogenic, Neoplasm, Congenital) -Onset < 72 hours -**Herpetic eye disease is the leading cause of INFECTIOUS corneal blindness in the US -1st refractive surface of eye = Tear Film; then cornea, anterior chamber, lens, vitreous, and retina -Corneal Edema = most common cause of increased intraocular pressure (IOP) -Mostly by acute angle closure glaucoma; becomes dull ground glass appearance -Acute Angle Closure Glaucoma -Acute onset, severe pain, mid-dilated fixed pupil could be irregular, ground glass appearance/cloudy, push on eye = rock hard, blurred vision, haloes around the lights, headache, nausea/vomit, IOP rises, shallow anterior chambers -Treatment = Pilocarpine 2% (muscarinic agonist), Acetazolamide (carbonic anhydrase inhibitor), Glycerine/Isosorbide, IV Mannitol (osmotic diuretic) -Also do a laser iridotomy to create a hole in the ciliary body to allow fluid to drain again -Treat both eyes at same timeprophylactic iridotomy if chamber is narrow; drugs are NOT substitutes for iridotomy -Hyphema = Blood in anterior chambermost commonly caused by blunt trauma -Decreased VA dependent on % hyphema -Hospitalize if > 2% hyphema/visiblere-bleed in 3-5 days. -sitting pt up leads to blood pooling in base of anterior chamber with a clear meniscus -Vitreous Hemorrhage = bleeding into vitreouslike a hyphema, but resolves slower -Looks like cobwebs/blobs; like blood in clear jelly -Most commonly caused by diabetic retinopathy + neovascularizationthen by retinal detachment -Dx made through dilated pupil -Vitreous Detachment = vitreous separates from retina with agingthe gel liquefies/shrinks/becomes opaque -Nearsighted (myopia) > Farsighted (hypermyopia) -When it pulls away, it makes specks/clumpsthese reflect shadows into retina -FLOATERS! -Etiologies = Myopia, Cataract surgery (YAG), Inflammatory disease -Retinal Detachment = Photopsia + Floaters -Hole in the eye, Fireworks in the eyeflashes of light -Followed by shade in visual field, slow loss of peripheral vision -Begins peripherally and dissects posteriorly -Dx through dilated pupil by ophthalmologist -Macular Diseasepoor vision, generally NOT RAPD (relative afferent pupillary defect) -DRUSEN BODIES! -Young pts = central serous retinopathy -Old pts = macular degeneration; dry vs wet -Sudden loss of vision if wet disciform -90% will have chronic form10% have sudden hemorrhage in choroid -Use Amsler Grid to help Dx -Amaurosis Fugax = sudden complete loss of vision lasting seconds to minutes; monocular dimming of vision -Temporary arterial obstruction; mini stroke/TIA of the eye -Evaluation: Cardiovascular, Cerebrovascular, Ophthalmologic, Migraine (ECHO, Holter monitor, etc.) -Scintillating Scotoma (a spot of flickering light near or in the center of the visual fields, which prevents vision within the scotoma )mostly from Migraine- heat waves/cracked mirror visual symptoms -Cant prevent -Like going into the fog -Migraine - Scintillating scotoma see above - Amaurosis fugax - Ransient cortical blindness - Homonymous hemianopsia - Classic or opthalmic

Lecture 4 - Acute Visual Loss II Vascular Occlusions--1. Central Retinal Artery Occlusion (CRAO) = EMERGENCY! requires skilled medical care in seconds-minutes! -Occlusion can be from: 1)cardiac, 2)talc, 3)fat, or 4)vasculi -The other ocular emergency is chemical burns -Sudden, painless visual loss w/RAPD (relative afferent pupillary defect) -Appearance depends on timing: -Mins-hrs: Boxcarringblood vessels barely moving -Hrs: Cherry Red Spot + Opaque Retina/Pale Disc -Bad light perception + Afferent defect -Treatment = digital message, glaucoma meds (take pressure off vessel), call ophthalmologist! 2. Branch Retinal Artery Occlusion (BRAO) -Branch of central artery involvedmore common associated w/ emboli -Could also see boxcarringscotoma depends on where the artery occlusion is -Source of embolus = Cardiac (#1), talc-IV, vasculitis, or fat -Scotoma depends on size and location 3. Central Retinal Vein Occlusion (CRVO) -Artery = pale Vein = cotton-wool spots, engorgement, disc edema -Severe vision loss > 50yo -Blood and Thunder appearancedisc edema, cloudy, diffuse retinal hemorrhages, venous engorgement, cotton wool spots -Etiology = HTN, Atherosclerosis, Diabetes, glaucoma, anything that will make it hyperviscous (smoking, etc) -Treatment = resolves spontaneously, monitor for neovascular glaucoma and open angle glaucoma 4. Branched Retinal Vein Occlusion (BRVO) -Generally noticed when it affects the macula at site where artery crosses vein causing macular edema -Etiology = Htn, Atherosclerosis, Diabetes, anything that will make it hyperviscous (smoking, etc) Optic Nerve Diseases--1. Optic Neuritis -Idiopathic inflammation of optic nerve; - Often associated w/ Multiple Sclerosis (#1) and post-viral infection - Classic sign = RAPD -Prognosis is good -Treatment = corticosteroids (IV), dont give orals a.) Papillitis = inflammation close to eye; swollen optic nerve (disc edema)/Inflammatory + RAPDAsymmetric! b.) Retrobulbar Neuritis = doesnt involve actual eye (behind eye so no disc edema) young adult w/ monocular loss of vision, Sharp/Crisp Optic Disc, and Pain on ocular movementcompressive optic neuropathy + RAPD 2. Papilledema Papillitis Papilledema -Vision is good, pupillary reflexes normal* Reduced Vision Normal -Disc swelling due to increased ICP...Bilateral! (disc RAPD Pupillary Responses Normal swelling is NOT papilledema w/o increased ICP) Swollen Optic Nerve Swollen -If chronic untreatedvision loss Present Hemorrhages Present 3. Anterior Ischemic Optic Neuropathy (AION) Inflammatory Etiology Raised ICP -Occlusion/Hypoperfusion of short post. Ciliary arteries = ischemia of optic nerve + altitudinal visual field defects (superior or inferior) -Etiology = Arteritis (inflammation) occlusive, Arteriosclerosis hypoperfusion and hypoxia a.) Arteritic Temporal Arteritis or Giant Cell Arteritis ->55yo, sudden loss of monocular vision (40% bilateral) -Long prodrome may precede visual loss -Cephalalgia (headache), Scalp Tenderness, Jaw Claudication (hurts to chew), Malaise, Weight Loss, Fever, Arthralgias (polymyalgia rheumatic = PMR), limb girdle pain, increased sedimentation rate -RAPD, Pale swelling of optic nerve, Altitudinal VF defect -Get STAT ESR! (>50 mm/hr is suggestive)then start high dose systemic steroids and get a temporal artery biopsy -Basically just treat people so they dont go blind in their other eye. Dont really help affected eye b.) Non-Arteritic same ocular findings but optic nerve NOT pale -Poor vision, RAPD, Altitudinal VF defects, swollen optic nerve with splinter hemorrhages -Normal ESR + Biopsy* = No Treatment! 4. Visual Pathways -Vascular occlusion in CNS = stroke, ischemic/hemorrhagic infarcts of pathway/cortex Trauma---Shearing of vascular supply from concussive forces, avulsion of optic nerve

-Pts usually present with RAPD, but wont see anything if you image these pts Functional Disorders---Exam is incompatible w/ symptoms (say they cant see but flinch when you put hand in face)malingering/hysterical Lecture 5 Chronic Vision Loss -Most common cause of blindness (US) = Diabetes > Macular Degeneration > Glaucoma -Most common surgery (US) = Cataract surgery 1.) Glaucoma -Most important cause of blindness in African Americans, blindness can be prevented, slow -TRIAD = IOP (normal = 10-21), Optic nerve damage ( cup:disc >0.5), Visual field loss -Asymmetry of cup;disc -Vertical elongation of optic nerve, disc hemorrhages, nasalization/excavation of vessels, notching of cup -Disparity of >0.15 of cup:disc = suspicion of glaucoma -Test w/ side penlight testiris bowed forward = shallow anterior chamber -4 Types: 1)Primary Open Angle, 2) Angle-Closure, 3) Congenital, 4) Secondary a.) Open Angle = most common (2/3), familial -trabecular meshwork gets clogged so fluid just cant get out; bilateral but asymmetric -Risk factors = >50yo, Family Hx, African American, Myopic -ASYMPTOMATICcommon, chronic, no pain/gradual elevation, normal pupil, no nausea; slight increase in IOP -Tx: -blockers (#2), Prostaglandin analogues -prost (#1), or surgery like laster trabeculoplasty or placement of aqueous drainage device b.) Angle Closure -Iris gets pushed up and blocks drainage area, so fluid has nowhere to go! -SYMPTOMATICuncommon, acute onset, ocular pain, blurred vision, haloes around lights, headache, nausea/vomiting, mid-dilated fixed pupil, ground glass, cloudy cornea, red eye, rock hard eye -Precipitating factors = stress, natural dilation of pupil, dilating drops, sympathomimetic drugs -Treatment = Pilocarpine, Acetozolamide, IV Mannitoltreat the other eye too! (prophylactic laser iridotomy). Mititotics are NOT a substitute for iridotomy -if suspected, refer to ophthalmologist immediately! c.) Congenital -dont miss this in a child with large eyes! -Refer if -IOP > 21 mm Hg, IOP not elevated by difference of > 5 mmHg, C:D > 0.5, C/D difference > 0.2, Symptoms of acute glaucoma, Congenital or secondary glaucoma 2. Cataracts -Normal aging process of lensonly needs surgery if patient wants it! -They diffuses the light entering the eye, leading to poor vision b/c you cant focus as well anymore -Correctable; most successful operation in all of surgery (and most common) remove lens and replace with implants -removal of primary lens/cataract usually with ultrasound, not laser. Removal of 2ndary cataract is w/laser -cant guarantee better vision post surgery, especially if macular disease is present -Blurred vision, increased myopia (dont need reading glasses), decreased colorsbrowner/yellower; poor red reflex -Refer when bad vision interferes w/ ADLspatient decides when to have surgery 3. Macular Degeneration -Leading cause of blindness in patients >55yo***Refer right away b/c possible Rx! deterioration of vision -Drusen Bodies (hyaline nodules in Bruchs membrane), retinal pigment epithelial atrophy, sub-retinal neovascular membranes (this is what causes acute loss in vision). -normally a progressive deterioration of vision ->C/D ratio or assymetry -Age Related MD -Atrophic (DRY) = gradual loss of vision + Drusen; no real Tx -Exudative (WET) = sudden loss of vision, subretinal neovascularization, accumulation of fluid + blood; can use laser therapy for this form (not a cure, but significant improvement) -Early in disease difficulty reading, driving, etc. Late in disease - Centrally blind with intact peripheral vision -Minimize bystop smoking, control cardio disease, diet high in fruits/vegetables, antioxidant vitamins w/ lutein - monitoring via Amsler grid; the appearance of the macula is a poor predictor of VA -Risk Factors = age, smoking, hyperopia, blue eyes, family hx, UV light -Usually no treatments, but can try Avastin or Lucentis -Thermal Laser surgery of NVM and low vision aids can be helpful in pts w/ ARMD only helps restore ~10% of vision -Basically just causes new vessels to coagulate and be destroyed; results in blind spots where Tx occurred. -Photodynamic Therapy dye administered by IV, cold laser activates dye in vasculature of eye, causes coagulation and destruction of abnormal vasculature -Avastatin and Lucentis block VEGF so no new vessels can be created; Avastatin much cheaper but off-label use -Just by looking at the macula is does NOT mean we can predict how well someone can see. -Points to Remember:

-glaucoma should be suspected if >C/D or asymmetry -both laser surgery of NVM, low vision aides, and motivation can be helpful in pts with ARMD Lecture 6 Red Eye I -Symptoms + Causes: -Itching = Allergy -Scratchiness = Foreign body, Dry eye -Burning = Lid, Conjunctival, Corneal disorder -Localized Tenderness = Stye, chalazion -Deep Intense Pain = Corneal abrasion, Iritis, Acute Glaucoma, Sinusitis -Photophobia = Corneal abrasion, Iritis, Acute Glaucoma -Halo Vision = Corneal edema -Exudates -Pus/Purulent = corneal ulcer (ciliary flush), bacterial conjunctivitis (diffuse) -White Stringy = allergic conjunctivitis (diffuse w/ exudate) -Serous/Watery = viral conjunctivitis -Preauricular lymphadenopathy = Adenovirus or Herpetic (viral conjunctivitis and VERY contagious) 1.) Cellulitis cant tell from pictures if eye is involved or not -Pre-Septal Cellulitis = child < 36mo associated w/ URI otitis media -Spread from contiguous lid infectionx-ray if trauma/sinus disease -Tx: Warm/moist compression + Systemic antibiotics -NO hospitalization -Orbital Cellulitis = 90% extensions from bacterial sinusitis -EOM motility is impaired + painful* - +/- Proptosis, +/- O.N. involvement (decreased vision, RAPD, disc edema) -External appearance will be red and swollen -Hospitalization, culture, start parenteral ABXs, consult ophthalmologist/ENT, if not better in 24 hrs get Radioimage sinuses via CT, IVtreat aggressively go to surgery if >24hrs of Tx w/o response -Usually immunocompromised pts if fungal involvement (DM, AIDS, CA, etc.); need surgical debridement 2.) Herpes Zoster -Intense pain in scalpprobably follows dermatome (1st div of CN V) -Itching, Photophobia if uveitis -Vesicles, Crusting w/ exudate, doesnt cross midline, occasional Conjunctivitis/keratitis/uveitis/glaucoma -Treatment = Oral ___clovir and/or capsaicin to reduce skin/ocular involvement; takes 1-3 months to get better 3.) Nasolacrimal Duct Obstruction a.) Congenital -30% of newborns affectedtearing and mattering most common; may also have dacryocystitis, amniotocele, or mucocele -80-90% resolve spontaneously w/in 8 months; so no surgery as a rule for a while -topical antibiotics, massage tear sac daily, probing, and irrigation; systemic ABXs if infected b.) Acquired -Often secondary to polyp/tumor; basically just dacryocystitis -Systemic antibiotics generally need...then surgery 4.) Blepharitis -Chronic Inflammation of lid margins -Staph, Seborrheic, or combo of the two -Foreign body sensation, burning, mattering -Can cause lid notching -Treatment = hygiene (warm/moist compress), antibiotic solution QID, antibiotic ointment at night -Often accompanied along with Acne Rosacea 5.) Acne Rosacea - Pustules, erythema, telangiectasia, rhinophyma -Rxn to staph Ags or abnormal sebaceous material (often seen with blepharitis) -Treat with tetracycline + erythromycin to decrease melting point of oils and help drain better 6.) Stye/Chalazion just lumps and bumps on the lid -Inflammation of glands of eyelid, external Zois/Moll glands, or internal Meibomian glands -Treatment = promote drainagewarm/moist compress w/antibiotic solution QID; incision with curettage if no response 7.) Ectropion/Entropion -Turned out/in eyelid; entropion a bit worse b/c lashes can scratch cornea leading to infection/ulcers -Burning, tearing, mattering, keratitis, ulcerstreat w/ antibiotic solution/ointment eventually will need surgery

Lecture 7 Red Eye II 1.) Conjunctivitis make sure to check both bulbar and palpebral areas a. Bacterial = Staph, Strep (both most common), Haemophilus, Pseudomonas (contact lens), Chlamydia trachomatouspurulent -DONT CULTURE b/c theres so many of these bugs as normal flora in the eye already! (Staph is the most common normal flora) -Often bilat, wake up in the morning with your eyes stuck shut, lid crusting, mucopurulent discharge -Treatment = Topical antibiotics drops (day)/ointment (night) + warm/moist compression - Use Tobramycin (aminoglycoside) and then Ciprofloxacin (fluoroquinolone) if it doesnt work -Pseudomonas is most common cause of central corneal ulcers in contact lens wearers b. Viral = Adenovirus (most common viral), Herpes is #2clear/serous/watery discharge -2nd most common cause of conjunctivitis; decreased VA d/t corneal infiltrates -5-12 day incubationtransfer via fomite/droplet (can live up to 28 days on surface) -Contagious for 10-12 days (VERY contagious) -often starts in one eye and moves to the other relatively quickly -Palpable preauricular node -Treatment = symptomatic relief via antihistamines, cool compression, NSAID, fluids, etc. No antibiotics b/c theyll send the kid back to school and infect everyone else! -Do NOT use topical corticosteroids! (can cause keratitis/ infection, cataracts, increased IOP) -Antivirals ineffective against Adenovirus -Herpetic Infections---dont treat them, refer! -Leading cause of infectious CORNEAL blindness in US -Many times due to improper use of topical steroids in undiagnosed herpes -Feels like a foreign body in eye -Type I > Type II -Initially a blepharoconjunctivitis (then dendritiform/stromal types) -Dx: Vesicles on skin/eyelid margin, Conjunctival follicular reaction (cobblestone of lower lid), Epithelial keratitis, Pre-auricular lymphadenopathy; see the epithelial dendrite in eye (hallmark) -Nearly everyone has serologic evidence of HSV -Treatment = oral antivirals, topical trifluorothymidine c. Allergies = most common cause of chronic conjunctivitisstringy/white mucus -5-25% of population, 70% of pts w/ seasonal allergies, impacts activities/emotions/appearance -Usually bilateral ocular itch, hyperemia, lid edema/puffiness, chemosis (conjunctival swelling), burning, stinging, tearing, photophobiatreat w/ antihistamine/decongestants/steroids (the best) -Papillary hypertrophy of tarsal conjunctiva (cobblestone pattern to papillae), EO/Mast cell d. Neonatal Conjunctivitis -If 1st month of lifeconsider venereal disease -Bacterial = Gonococcal (hyperacute purulent conjunctivitis), Staph, ChlamydialViral = Herpes e. Contact Lens-Induced Conjunctivitis -Type I and IV hypersensitivity -Treatment = clean contacts daily (H2O2 + enzyme tx), frequent replacement, change polymer, etc -pseudomonas f. Adult Chlamydial Conjunctivitis -Preauricular adenopathy, scant mucopurulent discharge -Prevalent in adolescents/young adults -Transmission via direct/indirect contact w/ genital secretions, cosmetics, swimming pools -1-2 weeks until onset -If lasts longer than 3 weeks, think of Chlamydia instead of Viral -Tx: Tetracycline or macrolide (azithromycin) for 3 weeks g. Ulcers all types of conjunctivitis can lead to ulcers/keratitis -Bacterial = staph, strep, pseudomonas (contact lens wearers); refer to ophthalmologist and Tx with fluoroquinolone h. Fungal Keratitis trauma during recreational or outdoor work activity with plant or dirt debris i. Acanthamoeba Keratitis parasitic infection of contact lens wearers using homemade saline, contaminated H 20, or corneal trauma -blurred vision, redness, tearing, photophobia, SEVERE pain 2.) Chemical Burns EMERGENCY! -1 of 2 ocular emergencies (this and CRAO)alkali more serious than acid -Treatment = IRRIGATE! topical anesthesia, then irrigate again, then PE to check for foreign bodies, cycloplegicthen topical antibiotic, pressure patch, referral 3.) Conjunctival Hemorrhage

4.)

5.)

6.)

7.)

8.)

9.)

-Looks bad, but usually harmlesscaused by sneezing/coughing/valsalva -Spontaneous resolution Inflamed Pinguecula/Pterygium -From UV + Wind exposure -Treatment = artificial tears, topical vasoconstrictors/antihistamines Episcleritis/Scleritis -Pain when pt moves eye, impaired EOM functioninflammation of sclera -Episcleritis is superficial, flat, benign -Scleritis is raised, hyperemic, associated w/ collagen vascular disease Dry Eyes (Dysfunctional Tear Syndromes) -Dry eyesburning, foreign body sensation, tearingcaused by aging, RA, meds, Steven-Johnson -Exposure Keratitis (Graves/Bells Palsy)incomplete lid closure tape shut at night but do NOT patch -One of the most commonly underdiagnosed ocular conditions in US (older women) -Association with connective tissue disease -Treatment = artificial tears, lubrication, punctual plugs arent effective for all pts. Use Restasis (cyclosporine); theres a lot of options for Tx, which means that none of them work very well Corneal Abrasion -Topical antibiotics and analgesics (NSAIDs) -Do NOT use topical anesthetics corneal toxicity!...NEVER prescribe (the inhibit growth/healing of epithelium, cause severe reactions, eliminate protective blink) -Do NOT use topical steroids! exacerbate Herpes Keratitis, etc. -MUST see them the next day! -think of abuse if cigarette burn Iritis -Photophobia, pain, miotic pupil (so much inflammation that the iris is clamping down), decreased vision, trauma, WBCs in the anterior chamber, Keratic precipitates -Dont use topical anesthetics or steroids! -recognize and refer Squamous Cell Carcinoma

<<<RED EYE points of interest>>> -If visual acuity acutely/significantly reducedconjunctivitis is unlikely -Check w/ fluorescein for epithelial defects -Pupil inequality is a danger sign for serious ocular disease -AVOID TOPICAL STEROIDS!! lead to: 1)exacerbation of Herpetic Keratitis, 2)elevated IOP, 3)cataracts, 4)potentiation of fungal corneal ulcers -DO NOT PRESCRIBE TOPICAL ANESTHETICS! They 1)inhibit growth & healing of the epithelium, 2)may cause allergic rxns, 3)eliminate protective blink exposing cornea to dehydration, injury, and infection. Lectures 8 and 9 Ocular Trauma -Teardrop pupil ALWAYS points to trauma -Types of wounds: -If hammering on metallook for intraocular foreign body or penetration -If grindinglook for corneal foreign body -If weldinglook for corneal UV burn -If playing a racquet sportlook for hyphema, blowout fracture, ruptured globe -Types of Emergencies: -True emergencies = chemical burns (irrigate) + CRAO (orbital massage) treat w/in minutes -Urgent = conjunctival/corneal foreign bodies/abrasions, penetrating injuries, lid lacerations, hyphema, radiant energy burns, traumatic optic neuropathy treat w/in hours -Semi-Urgent = orbital fractures, subconjunctival hemorrhages treat w/in days -Treatment = irrigation, foreign body removal, medicate, patch, suture; -Tetanus booster if wound is dirty and >5years since last one or if wound is clean and >10 years since last one -Avoid digital palpation in suspected trauma (especially if globe could be ruptured) -Do NOT patch ifcontact lens wearer, dendritic/stellate epithelial defects, poor historians -Follow up in 24 hours -Do NOT use topical anesthetics! 1.) Chemical Burns -Alkali more serious than acid, immediate irrigation is essential -Treatment = topical anesthetic (so they keep eye open), then irrigate, then check for foreign bodies, copious irrigation -Follow up with topical cycloplegic agent (ciliary paralysis), then topical antibiotic, pressure patch, and referal 2.) Corneal Abrasions -Foreign body sensation, SEVERE PAIN, tearing, photophobia -Treatment = topical cycloplegic/antibiotic, pressure patch, topical analgesia (not anesthetic), etc

-cycloplegic = ciliary paralytic agent -DO NOT patch a contact lens wearer b/c its more than likely an ulcer! usually caused by pseudomonas -Follow-up in 24hrs. If its not healed, refer to ophthalmologist b/c theres something else wrong! 3.) Globe Rupture/Laceration -Shield it (not patch) and refer!...probably shouldnt do an MRI; get an X-ray at minimum or do a CT -If the Globe is ruptured or a Laceration is suspectedstop exam, shield eye (DONT PATCH), give tetanus prophylaxis, refer 4.) Hyphema -Assume that the globe is rupturedshield it and send em out -25% have other ocular injuries -Tend to re-bleed in 3-5 days (into anterior chamber) -Can have glaucoma complication 5.) Severe Orbital Hemorrhage -Apply anesthetic, clamp lateral portion of eye with hemostat, and cut (lateral canthotomy) allows decreased pressure and drainage -Bulous subconjunctival hemorrhage, proptosis, corneal exposure, elevated IOP 6.) Orbital Fracture -Periorbital edema, ecchymosis, diplopia, subcutaneous emphysema, hypesthesia -Surgery ifpersistent diplopia or poor cosmesis (enophthalmos) 7.) Superficial Lid Laceration -If lid margin is involved do NOT fix it!...refer. if you try to fix it theyll always tear up b/c their drainage system has been compromised -Remove foreign body, rule out deep foreign body, give tetanus prophylaxis 8.) Ultraviolet Keratitis -Welders burn, snow blindnesscornea is highly susceptible to UV rays -Pain, foreign body sensation, tearing, photophobia -Treat with patch, cycloplegics, topical analgesics (NSAIDs) 9.) Traumatic Optic Neuropathy -Direct (laceration of ON on bone) and Indirect (shearing forces) see notepool -Shearing force on optic nerve/vascular supply -Visual loss is severe/immediate, RAPD! (do swinging penlight) -Treatment = neuroimaging, orbit/cranial surgery if direct, prognosis is poor 10.) Conjunctival Hemorrhage looks bad, but is harmless; ensure spontaneous resolution and assurance to pt -D/t sneezing, coughing, valsalva 11.) Acute Glaucoma -Fixed, Mid-Dilated pupil, rock hard, painful, red eye 12.) CRAO -True emergency, sudden/painless visual loss, do not delay, treat w/ digital message/glaucoma meds/refer -Blind eye w/ pale disc, cherry red spot 13.) Anterior Ischemic Optic Neuropathy Arteritic -Temporal Arteritis, Great Cell Arteritis>50 ESR suggestive, use high dose steroids, get biopsy 14.) Orbital Cellulitis -Red/swelling external, impaired EOM motility, painful, proptosis, decreased vision, RAPD, disc edema -HospitalizeIV antibiotics Important Points for Trauma -Teardrop pupil, avoid digital palpation, papillary dilation, chemical burn irrigate, never do MRI on metallic foreign object, never Rx topical anesthetic

Lecture 10 Amblyopia and Strabismus -Amblyopia (lazy eye) = abnormal visual development/suppression; decrease in vision (not misalignment!) -Decreased visual acuity is uncorrectable with glasses; can be prevented if caught early! -Unilateral > Bilateral (bilat could mean effective blindness) -2-4% of population; Familial -Vision is developmental poor at birth, normal acuity at 3yo (vision wont develop w/out proper vision-receptive stimulation) -Failure of developmental process, not organic abnormality and therefore treatable and preventable -As such, heretofore, one must detect it early in life!...then patch -Treatment should begin before 5yolikely ineffective past 10yo ->50% of amplyopic pts have strabismus (misalignment of eyes) = lazy eye -Brain selects/favors the aligned or least blurred image and suppresses the blurred/conflicting image causing a lazy eye. -Predisposing factors = poor aim (strabismic amblyopia), poor focus (refractive amblyopia), poor clarity (occlusive amblyopia) -Unilateral AmblyopiaFailed vision test, strabismus, parental concern -Detection: Assess red reflex, determine visual acuity, evaluate ocular alignment -Treatment: PCP detects it, Ophthalmologist treats it -optimize the retinal image clear the visual pathway (cataracts or ptosis Sx), correct the refractive error (glasses vs contacts) -intensify the neural image to the visual cortex occlusion therapy (full-time vs part-time), atropine penalization therapy, optical graduation with opaque contact or ND filters -Occlusion therapy = occlusion of good eye (dont patch too long though) -success of occlusion therapy is dependent on age, degree of amblyopia, and compliance of child (dependent on parents). Must continue use through pts first decade of life and follow through teen years. --Does NOT eliminate strabismus! -Atropine Penalization Therapy = morning drop of 1% in good eyecant accommodate for near vision (can still use for distance) -Strabismus = misalignment of the two eyes -Paralytic (incomitant) or Non-Paralytic (concomitantangle of deviation constant in all gazes) -Tropia = manifest -Phoria = latent/fusion interrupted -Direction (Eso = inward, Exo = outward, Hyper = up, Hypo = down) -Diplopia is absent in kids! they are only seeing out of one eye (brain suppresses the other one) -Testing: Cover/Uncover test best for EOM function; epicanthal folds, different facies, corneal light reflex -EOM uncoordinated up to 3-4 months in newborn; after 4 months of age their eyes should be coordinated -Always do red reflex -Glasses alone correct some forms of strabismus, EOM surgery may be necessary (wont correct binocular vision, but will correct disfiguring strabismus) -present with failed vision test, strabismus, and/or parental concern -Treatment: -glasses alone can correct some forms of strabismus -EOM surgery may often be necessitated but wont correct binocular vision (will correct disfiguring strabismus and help with self-image) -treat amblyopia before EOM surgery -vision training has no proven value in amblyopia or strabismus; a crock of fecal matter -Retinopathy of Prematurity -Retina is vascularized from optic disk in 24 weeks; more premature infant, less vascularization. Developing peripheral vessels are arrested by excessive O2. Then ischemic damage to peripheral retina can occur leading to vasoproliferation which causes fibrosis and retinal detachment. -These kids need to be followed closely by an ophthalmologist. Initial exam at 4 weeks, then every 2-3 weeks -Referral immediately ifpoor red reflex, parental concern, asymmetric/diminishing visual acuity, constant/acute-onset strabismus -Less emergent referral intermittent strabismus on exam, persistent parental concern, associated syndromes or systemic disease -Leukocoria white pupils; bad sign; could be retinoblastoma -Newborn Exam: -corneal light reflex -red reflex -pupillary reflex (sluggish is normal) -if possible fundus exam -EOM may be uncoordinated for 3-4 months

10

-Infant Exam: -fixes and follows an object of interest (toy for example), head turn, for EOM testing -central, steady, & maintained red reflex/gaze; smile @ child, if they smile back they can see out of at least one eye -cover good eye, how does child react? Protest? Cry or evasive action? They should be try to get away and be upset that youve covered their good eye(s) if the other eye has a problem 2-4 Year Olds: -3year old may perform E game, Allen pictures -if less than 20/40 refer -cover/uncover test -Photo screener? Not a substitute for visual acuity -Child: -usually Snellen -may perform E game -if less than 20/40 refer -cover/uncover test -Additional Tests -red reflex perform in all infants and children -ophthalmoscopy mandatory for any pt w/reduced vision or strabismus -pupillary reaction may indicate neurologic disease ***Important Points*** -Amblyopia must be detected early -Both amblyopia and strabismus have strong family histories -VA testing is very important -Amblyopia can present without strabismus -Serious conditions can cause strabismus -If poor red reflex, poor vision, or large eyes refer -KIDS DONT SEE DOUBLE Lectures 11 & 12 Neuro Ophthalmology I & II -35% sensory fibers going into brain are in optic nerves -65% of intracranial disease have neuron-ophtho signs/symptoms -RAPDuse swinging flashlight test (the most important optic test you can do) -Pupil Disorders 1.) Dilated Pupil -Efferent defect (CN III) -can be pupil sparing (dilated pupil). This is b/c pupillary fibers are on the periphery of CNIII. If a tumor pushes on the nerve, these fibers will be more affected than the inner fibers, leading to pupillary dilation. -In vascular diseases (like DM), the inside fibers will be more affected and the EOMs will be affected while the pupillary fibers will be spared (normal pupils) -EOM paresis/palsy (LR unopposedso aBducted) -Adies Tonic Pupil pupil does not react and is slightly irregular (egg-shaped) -Blurred near vision, periocular discomfort, decreased depth perception -70% female, 80% unilateral -Associated w/ weak deep tendon reflexes -pupil has super-sensitivity to pilocarpine (muscarinic agonist) (HALLMARK) -Pharmacologic pupil -Traumatic Mydriasis 2.) Unilateral Small Pupil -Physiologic Anisocoria (different sized pupils) 20% -Horners Syndrome -Sympathetic pathway lesion, TRIAD = Ptosis (via messed up Muellers muscle), Miosis, Facial Anhidrosis (lack of sweating); may also see heterochromia (different colored eyes) if congenital -Levator is NOT involved (its the Muellers muscle). B/c its an SNS pathway -Pathway hypothalamus C7-T2 carotid bifurcation eye; putting in central lines can cause hemorrhage that affects this pathway; also Pancoast tumor -Argyll Robertson Pupil (Prostitutes pupil) -Pupils accommodate but do NOT react to light -Pupils irregular and small, usually bilateral, -Associated w/syphilis, Diabetes (most common), Alcoholism -Two types of lesions:

11

-Vascular DM, HTN, etc; leads to (see notepool) -Impingement aneurysm, tumor, etc; leads to permanent dilation of pupil that is not reactive to light -EOM Disorders: you CAN have diplopia w/one eye (ghost images) -CN III Paresis = Skewed/Oblique -EOM abduction, horizontal and vertical diplopia (skewed), ptosis -pupil may or may not be dilated depending on if vascular or compressive problem -CN IV Paresis = Vertical oblique diplopia and compensatory head tilt to opposite shoulder that makes diplopia go away -most often caused by closed cranial trauma -CN VI Paresis = Loss of aBduction (could be caused by pseudotumor cerebriincreased intracranial pressure) -Horizontal diplopia -CN V Paresis = check cornea w/cotton wisp and sharp/dull facial sensation; cant be wearing contacts -CN VII eyes will always be open b/c this nerve usually closes the eyes; facial muscle weakness -CN VIII can you hear me? -Myasthenia Gravis = Great imitator (can mimic any of the CN palsies) -Chronic autoimmuneptosis/diplopia in 50%. Also fatigability w/o pupillary abnormalities that get worse as day progresses -Common causes of diplopia = CN III/IV/VI palsy, MG, Graves, Blowout fracture -Nystagmus = dancing eyenamed for fast component -Benign Types: 1) endpoint/physiologic/normal occurs at extremes of EOM movement 2) drug induced barbiturates, diphenylhydantoin (dilantin) 3) congenital, -Congenital Anomalies of the Optic Nerve: Blurred disc margins, pseudopapilledema nothing wrong with these people -Papilledema = disc edema from increased intracranial pressure (NOT just disc edema in-and-of itself) -Hyperemia (blood flow) of disc, tortuosity of vessels, blurring + elevated disc, bilateral, good vision until chronic -NO Spontaneous Venous Pulsations (SVP) check for these with anyone that c/o a headache -From brain tumors (50%), pseudotumor cerebri (also see CN VI lesions), severe HTN -Papillitis = inflammatory edema of disc; maybe associated with MS? -Hyperemia, tortuosity, blurring + elevation, unilateral/asymmetric, RAPD, poor vision -Optic Atrophy (atrophy of CN II) -Pallor of optic disc, progressive loss of axons, could be chalk-white if extensive (from normal pink color to chalk white) -Dx only if decreased VA or VF or if unilateral RAPD -Caused byprevious optic neuritis (seen in MS), long-standing papilledema, compression of optic nerve, ischemic damage, glaucoma, previous optic nerve trauma, toxins -Visual Field Defects -Scotoma = reduced/absent vision, Hemianopia = loss of VF, Homonymous = R or L VF loss -Ant. to Chiasm = Monocular; Chiasmal = Bitemporal Hemi; Post. Chiasm = Homonymous Hemi; -Visual Hallucinations (Charles Bonnet syndrome) --- Cognitive Visual Loss (AD, simultagnosia, clock drawing) -elderly pts, significant visual loss (<20/100), cognitively intact with appropriate LOC, repeated, formed visual hallucinations often vertical or horizontal; usually pleasant and interesting hallucinations; pts aware that these are not real ***Points to Remember*** -Test VA and VF if abnormal ON -If unilateral ON lesionequal pupils but RAPD -Blurred disc is NOT always papilledema -Chiasmal lesion = bitemporal hemi -Check other CNs if abnormal pupil/lid -Slow progression of visual lossconsider tumor/compression -Abrupt visual lossischemia/vasospasm/vascular. -Check CN V and VII if abnormal EOM and suspect palsy

12

Lectures 13 & 14 Manifestations of Systemic Disease I & II 1.) Diabetic Retinopathy -Leading cause of new blindness (20-74yo) -90% Type II -Ocular changes = refractive error changes, cataracts, retinopathy (most important) -Severity of retinopathy correlates with: 1) duration of DM, 2) HTN, 3) glycosylated Hg levels, 4) smoking (QUIT!) -Pathogenesis: glucose VEGF cap permeability/abnormal vasoproliferation -Diabetic visual loss can occur in all 3 types (Macular edema can be in any of these 3treatment = laser photocoagulationreduces visual loss by 50%) -Prevention of Macular Edema: 1) Control Hgb A1c levels, 2) proteinuria, 3) control BP w/diuretics and ACEIs/ARBs, 4) control serum lipids -Diabetics need to be screened by ophthalmologists every year, not FPs! -DM Pregos: ophtho exam before conception, then at 3 mo intervals beginning in 1st trimester -1/3 miss annual ocular exam, 60% miss laser surgerypoor pts a. Non-Proliferative Diabetic Retinopathy (NPDR) -Retinal blood vessels leak (if into macula, vision will be reduced)Can be asymptomatic -Vision loss from macular edema w/ hard exudatesfluid between rods/cones, not treatable if ischemic -2 causes of visual loss = 1) Ischemic Maculopathy (irreversible) and 2) Macular Edema (treatable) -Macular edema can be treated with laser photocoagulation which can reduce visual loss by >50%! May also use Triamcinolone injections -Characteristics: Microaneurysms, leakage of intravascular fluids (hard exudates), intraretinal hemorrhages (dot and blot), retinal ischemia (cotton wool spot = HALLMARK!) b.) Pre-Proliferative (Advanced Nonproliferative Diabetic Retinopathy) -Cotton wool spotsretinal ischemia, Capillary dropout, Venous beading (Sausaging) -Laser therapy can prevent long-term visual loss c.) Proliferative Diabetic Retinopathy (PDR) -Neovascularization (fine/wispy blood vessels from tissue hypoxia), Vitreous Hemorrhage (cobwebs/floaters), Traction Retinal Detachment, Fibrous proliferationcan also have NPDR findings (w/ macular edema) -Shows many fine, wispy vessels that are new d/t neovascularization d/t ischemia -Risk factor for MI, stroke, amputation, and death -Vision loss from 1) vitreous hemorrhages and 2) retinal detachment -Treatment = Laser Photocoagulation leads to involution of the neovascularization in the periphery; most effective before visual loss occurs! Prevents further neovascularization; spare the macula -Side Effects = constriction of peripheral VF, decreased night vision/near vision/central vision -Treatment for vitreous hemorrhage/retinal detachment = Vitrectomy- removal of jelly from eye -Complications = 50% will develop a cataract 2.) Hypertensive Retinopathy -High BP = constriction of arterioles -Severe rise (diastolic >120) leads to fibrinoid necrosis causing exudates), flame hemorrhages (2nd worst sign), can have Copper-Wiring -Malignant Htn = optic nerve disc edema (1st worst sign of HTN Retinopathy)looks like papilledema -Difficult to differentiate between chronic HTN and normal age-related changes -Attenuation of arterioles, Focal narrowing, AV changes -The higher the grade, the worse the diseaseGrade 4 includes disc edema! 3.) Arteriolar Sclerosis -Lead Pipe vesselsaccelerated by systemic HTN -Copper-Wiringseen at the AV crossing angles at high grades as walls of vasculature get thicker (3/4) -Silver-Wiringsame as copper-wiring but even thicker vasculature! Worst sign of arteriolar sclerosis -A/V Nickingarterioles and veins share common adventitial sheath at crossing sites, as arterioles become thicker, they push down on the veins causing nickingat high grades (3/4) 4.) Autoimmune Disorders a.) Thyroid Disease -Lid retraction/lag, exophthalmos (d/t EOM hypertrophy), conjunctival congestion, corneal damage -Not always correlated w/ serum thyroid levelscan progress after thyroid function is normal -Treatment = tear substitutes, corticosteroids, orbital irradiation/surgical decompression (no test Q on this) -Can also do lid/muscle/orbital surgery if in Cicatrical phase -Can injure optic nerve in thyroid disease by overstretching or compression -0-6 = NOSPECSwith last S being sight loss; you can get corneal damage and loss of vision! b.) Connective Tissue Disorders, Rheumatologic Disorders, and Others -DRY EYES (dysfunctional tear syndrome) are most common manifestationtreat w/ artificial tears, ointment, topical anti-inflammatory, fish/flax seed oil (omega-3s), punctual occlusion

13

-Sjogrens Syndrome = dry eyes, dry mouth, +/- connective tissue disorder -Rheumatoid Arthritis = dry eyes (most common), episcleritis, scleritis, corneal ulcers -Treat by getting disease and inflammation under control! -Juvenile Rheumatoid Arthritis = Iritis (10%, most common in pauciarticular, often asymptomatic/chronic white eye/not red)can lead to cataracts/glaucoma/corneal calcification -Systemic Lupus Erythematosus = dry eyes, scleritis, peripheral corneal ulcers, retinopathy (affects retina more than optic nerve)Cotton Wool Spots (retinal ischemia) -Ankylosing Spondylitis = photophobia, redness, decreased vision, iritis (refer) -Polyarteritis Nodosa = dry eyes, corneal ulcers, scleritis, HTN retinopathy, retinal vasculitis -Giant Cell Arteritis = headache, scalp tenderness, jaw claudication (hurts to chew), polymyalgia rheumatica -STAT ESR!, then start steroids if ESR >50, then Temporal Artery Biopsy -Begin treatment IMMEDIATELY w/ high-dose steroidsdont wait for biopsy results -Myasthenia Gravis = 50% have ptosis/strabismus, symptoms get worse when patient is tired -Sarcoidosis = chronic inflammatory, multisystem, focal/non-caseating granuloma, hilar lymphadenopathy, most common in African American women (20-40yo), Granulomatous uveitis, Candlewax Drippings/mutton fat inside cornea, dry eye syndrome. Refer these pts so they can start corticosteroid Tx. -Migraines = scintillating scotoma, amaurosis fugax, transient cortical blindness, homonymous hemianopia -Amaurosis Fugax = temporary arterial obstruction, sudden transient visual loss, monocular dimming of vision -Evaluate cardiovascular, cerebrovascular, eyes, and migraine symptoms for signs of throwing clots -Blood Dyscrasias = Hyperviscosity Syndrome (amaurosis fugax), Thrombocytopenia, Anemia/Sickle Cell -Central Retinal Artery Occlusion CRAO (EMERGENCY!) = Cherry Red Spot, retina, RAPD -Malignancy = mets most common malignancy (5% of autopsies); chemotherapeutic agents have lots of toxicities to the eyes like superficial keratitis, optic neuropathy, and CRAO! -AIDS = Cotton Wool Spots (most common ocular manifestation from Ag-Ab complexes occluding vessels), CMV retinitis (most common cause of blindnessBRUSH FIREoccurs when <100 cells/ml) -Syphilis can be seen in these pts when CD4 >100 cells/mL -Candidiasis = fluffy, white-yellow, superficial retinal or vitreal infiltrate; Tx with amphotericin B; seen in ICU pts -Herpes Zoster Ophthalmicus = intense pain/itching/photophobia, vesicles, crusting, spares midline, conjunctivitis, keratitis, uveitis, glaucomabe able to recognize it for the picture portion of the test. Lectures 15 & 16 Drugs of the Eye I & II -Eye can only hold drop, so put one in, wait, and then add another if necessary. If added too quickly, youll just wash the first drop out with the 2nd. Punctal occlusion occlude tear drain so drops stay in eye longer and have time to work. -Meds for Dx: -Topical Fluroescein for IOP, corneal abrasion, epithelial defects --- IV for retinal disorders - Can also be injected for a fluorescein angiogram to see if any bleeding in the eye -Topical Anesthetics for IOP measurements, superficial surgery, eval of painful eye --- these are the ___caines -Proparacaine, Tetracaine, Lidocaine -NEVER prescribe these b/c they are very toxic to the cornea!!!!! -Pupillary Dilationcholinergic blockers (get rid of atropine from your office)anti-SLUDE side-effects -Cholinergic Blockers - Parasympatholytic agents (Tropicamide) other agents (atropine/scopolamine) have too long of durations; work on the iris sphincter -Toxicity to these leads to mad as a hatter, red as a beat, hot as a -Adrenergic Stimulants - Sympathomimetic agents stimulate iris dilator, no effect on accommodation, can cause angle-closure glaucoma; Phenylephrine; ONLY ophthalmologist should ever use this! -Topical drops are best way to deliver med to cul-de-sacjust 1 drop! -can also use ointment (just 1/8 of an inch and only at night!), wafers, injections -Allergic Conjunctivitis the most common type of conjunctivitis in Iowa -Treat w/ tear substitutes, decongestants (not as a monotherapy), antihistamines/mast cell stabilizers (must be used all of the time b/c they take 3-4 days before they work), NSAIDS, corticosteroids (the best but should be used very cautiously) -Bacterial Conjuntivitis ___mycinAminoglycosides (neomycin is the #1 eye drug people are allergic to), Sulfonamides, Bacitracin, Fluoroquinolones (these are the big guns and should only be used for wicked infections) -Viral Conjuntivitis symptomatic relief with antihistamines, antibiotics (possible secondary infections), cool compress, etc. -Use caution w/ topical steroids - exacerbates Herpes keratitis, elevates IOP, cataracts -antivirals ineffective against adenovirus -Avoid close contact b/c VERY contagious -Herpes Simplex Keratitis = most common infectious corneal blindness in UStreat w/referral to ophtho (dont treat yourself!) -Avoid topical steroids - exacerbates Herpes keratitis, elevates IOP, cataracts -Herpes Zoster (Shingles) = use the ___clovirs which are oral antivirals - reduce risk of skin and ocular involvement and post-herpetic neuralgias -Uveitis iris + choroid + ciliary body inflammation treat with steroids -Open-Angle Glaucoma = treat w/ -blockers (depression, impotence, lethargy, etc.), carbonic anhydrase inhibitors, and prostaglandin analogues (#1) -**Prostaglandin Analogue Side Effects minimal, iris pigmentation, hypertrichosis (long eye-lashes), macular edema

14

-Open-Angle is asymptomatic in early states -Carbonic Anhydrase Inhibitors can cause hypokalemia, numbness/tingling, anorexia (food tastes like crap) -combination products contain B-Blocker + something else Side Effect IRREVERSIBLE SIDE EFFECTS @ Recommended Dosages Corticosteroids -Cataracts -Glaucoma Hydorxycholroquine/Choloroquine -Bulls Eye Maculopathy Topiramate -Angle-Closure Glaucomanot relieved by iridectomy Ethambutol (TB drug) -Dose-related Optic Neuropathy (know picture of optic atrophy) Amiodarone -insidious onset often bilateral A1-adrenoceptor blockers -Intraoperative floppy iris syndrome REVERSIBLE SIDE EFFECTS @ Recommended Dosages Anticholinergics -Decreased near vision, pupillary dilation, glaucoma Isotretinoin (Acutane) -Conjunctivitis, dry eye, cataracts, optic neuropathy Amiodarone -Corneal Whorl Dystrophy Chlorpromazine -Corneal/lens changes Bisphosphonates (osteoclast inhib.) -Red eye, photophobia (iritis), deep pain Statins -myopathy, diplopia, ptosis, Cataracts Rifabutin -Uveitis Sildenafil/Tadalafil Viagra/Cialis -Blue color tinge to vision, optic atrophy TNF Inhibitors -sensory neuropathy, Guillanin-Barre If above recommended dosages Reversible: -Digitalis = blurred vision, chromatopsia (yellow), fatigue/weakness -Diphenylhydantoin = nystagmus -Thioridazine = pigmentary retinopathy Important things to Know: - make sure to get the drugs in the cul-de-sac - never Rx or dispense topical anesthetics - never use Atropine or Scopolamine to dilate eyes - never Rx ocular steroids w/o precise Dx and be prepared to monitor for SE of cataracts and glaucoma Drug

Condition Proptosis/ Exophthalmos

Example

~LIDS~ Condition Periorbital Edema

Example

Retraction

Hordeolum/Sty

Ptosis

Xanthelasma

Ectropion

Dacryocystitis

Entropion

Herniated Fat

Epicanthus

15

Condition Conjunctivitis

~CONJUCTIVA + SCLERA~ *Zones of Conjunctiva = Tarsal along lidBulbar along eye* Conjunctiva starts on line of the lid and then reflects back onto the globe Example Condition Example Pterygium

Episcleritis/ Scleritis

Hemorrhage

Pingueculae

Condition Corneal Abrasion

~CORNEA/ANTERIOR CHAMBER~ CORNEA Example Condition ANTERIOR CHAMBER Example Hyphema (RBCs)

Keratitis/ Opacification

Hypopyon (WBCs)

Arcus Corneae

Iris Lesions

16

~FUNDUS~ Condition Pigmented Ring Example Condition Disc Edema Example

Scleral Crescent

Flame Hemorrhage

Myelinated Nerve Fibers

Dot and Blot Hemorrhage

Cup/Disc Ratio

Preretinal Hemorrhage

Arteriovenous (A/V) Crossing

Hard Exudates

Neovascularization

Chorioretinitis

Drusen -Hallmark of macular degeneration

Cupping

Cotton Wool Spots d/t ischemic infarcts

17

RANDOM PICTURES

Congenital Glaucoma Orbital Cellulitis

Hyphema

Herpes Zoster CRAO

BRAO

Nasolacrimal Duct Obstruction

CVRO

Blepharitis

Papillitis Stye + Chalazion

Macular Degeneration

Herpes

Pre-Septal Cellulitis

18

NastinessSevere Orbital Hemorrhage

19