ophtho

• absense of the eye
• seen in pigs with vitamin A deficiency

• normal eye but small
• seen in pigs with vitamin A deficiency

• a small eye with abnormalities
• seen in pigs with vitamin A deficiency

• removal of the whole globe
• within periorbita

• removal of the contents of the orbit
• most common
• external to periorbita

• removal of the contents of the globe
• put in prosthetic - can be done with heathy cornea.

• blind and painful (glaucoma or uveitis that O can't treat)
• severly damaged eye with loss of contents or high risk of infection
• intraocular neoplasia
• Carefully close periorbita CT to prevent sinking, or can use bowler hat prosthetic (NOT in neoplasia or infection)

• very thin bony shelf on floor of orbit
• Very thin medial wall in MANY species
• bones are paper-thin, and can cause emphysema or infection!!

• cavity in the skull containing the eye, supporting structures and other important structures
• floor is incomplete, "open" to the oral cavity in most species (cows have paper thin floor)
• Diseases nearby (sinus or teeth) can manifest in orbit
• full of the periorbita
• temporalis and masseter are walls.  If they atrophy eye sinks.  if they hypertrophy, exophthalmos.  
• Dehydration or starvation collapse fat pad, enophthalmos
• ramus of mandible right behind eye, so inflammation of orbit, hurts to open the mouth!  And mandibular tumor could push on eye

maxillary artery and deep facial vein run along orbit, don't cut them!!

• proptosis (this IS exophthalmos)
• CHANG (space-occupying lesions - cyst, hematoma, abscess, neoplasia, granuloma
• myositis/myopathy (acute) of masticatory muscles
• emphysema
• GLAUCOMA/BUPHTHALMOS (cow-eyed, enlarged) !!

• ocular pain (suck back when hurts)
• dehydration (fat)
• emaciation (fat)
• myositis/myopathy (chronic, atrophy)
• trauma
• Horner's (usu other signs, symp fibers in periorbita keep constricted)
• neoplasia in anterior orbit
• zygomatic mucocoele in anterior orbit
• emphysema
• SMALL GLOBE (rupture, microphthalmos, phthisis bulbi)

• EMERGENCY
• peracute to acute, rapid progression, sick and painful, exophthalmos, lid and periorbital swelling, red eye (chemosis, hyperemia), abnormal d/c, pain opening mouth
• no particular signalment
• don't differentiate cellulitis vs abscess, tx is same! idiopathic in dogs/cats, trauma (recent or old), extension from sinuses, FB (oral cavity, conjunctival or facial), tooth root abscess or recent dental in brachycephalic dogs and cats
• abx +/- tarsorrhaphy (sew eyelids together to protect), NSAIDs, analgesics, soft food, hot packs

• primary in orbit, metastatic or an extension from other tissues
• 90+% malignant, adenocarcinoma most common
• usu older animals, progressive changes
• minimal to no pain at early (unless VERY fast)
• unilateral
• sx extirpation, enucleation or exteneration, chemo, radiation (?)
• usu poor px because disease ADVANCED before we find it--lots of space behind the eye

• UNCOMMON but happens in SA
• HUGELY important to dx and tx early.  
• no retropulsion, exophthalmos, prolapse, cheek, temporalis swollen and painful
• autoimmune inflammatory disease of muscles innervated by mandibular nerve (masseter, temporalis, pterygoids, rostral digastricus).  
• Post-vax or infection?  aka atrophic myositis
• usu large breed dogs (only dogs), 3 years (<1 in CKCS)
• swelling/pain of those muscles, can't open mouth or pain (jaw hang open?), SOME have eye signs (usu bilateral exophthalmos, nictitans protrusion, periorbital/lid edema, conjunctival and episcleral vascular engorgement, blindness?, hypersalivation?  reluctant to eat or drink, clinical signs 2-3 weeks, recurrs frequently
• chronic: atrophy of muscles, can't open mouth/trismus, enopthalmos with entropion, nictitans prolapse, other immune diseases?
• run circulating ab test and/or ELISA (both) or biopsy temporalis or masseter - make sure you're deep
• ON EXAM
• TX: steroids, immune-modulatory if can't use steroids, PT and supportive, monitor for relapse.  DO NOT rip jaw open under anesthesia!

• no signalment, etiology unknown, slow or fast onset, minimal pain, signs vary with position.  
• swelling of orbit, exophthalmos or enophthalmos or deviated globe, nictitans protrusion, ventral or temporal fornix swollen and lobulated cyst visible
• aspirate - thick!  
• tx with abx, but usu need sx to remove gland (zygomatic)

• common in horses
• acute, pain, orbital swelling, chemosis (conj edema), exo or enophthalmos, SQ and conjunctival emphysema, bony irregularities, crepitus, epistaxis
• simple fractures that aren't displaced can avoid sx.  Abx, tx ocular PRN, TETANUS in equine, emphysema common (resolves slowly)

• RARE
• hugely popping out bilateral eyeballs!  unmissable presentation - increased scleral exposure, exotropia (lateral strabismus), epiphora (tearing), conjunctivitis.  NOT PAINFUL, seem happy.  Esp goldens, intact females, <3yo
• tx with steroids

• skin
• muscle: orbicularis oculi (ring around eye), levator palpebrae superioris (pulls eyelid up)
• tarsus/tarsal plate: CT surrounding tarsal glands, MUST close this layer in repair!
• palpebral conjunctiva
• medial and lateral canthal ligaments on the corners

• T-shaped cartilage with harderian gland, aqueous.
• prolapses with Horners (cows - ipsilateral dry nose, horses sweat), may have red eye from loss of vasoconstriction
• palpebral and bulbar surfaces covered with conjunctiva

• tri-layered
• lipid on top - tarsal glands, prevent evaporation
• aqueous (largest) - lacrimal glands, nutrients and waste
• mucin on bottom - conjunctival goblet cells, adhere to corneal surface

• stratified squamous to stratified columnar epithelial mucous membrane with LOTS of goblet cells, esp in fornices
• subdivisions: palpebral (inside of eyelids) vs bulbar (outside of the globe to limbus).
• transitions to cornea at the LIMBUS
• conjunctival sac is the potential space inside closed lids

• outer: fibrous = sclera + cornea, lamina cribrosa for ocular nerve to exit (sieve). Sclera continuous with dura mater around optic nerve
• middle: vascular = iris, ciliary body, choroid (continuous with pia mater around optic nerve)
• inner: neural = retina (formed by optic cup)

• 4 layers plus tear film.  
• 1. epithelial (+ basement membrane, hydrophobic), 2. stroma, biggest (hydrophilic). 3. descemet's membrane (hydrophobic). 4. posterior epithelium or endothelium (hydrophobic, pumps to maintain dehydration of stroma)
• transparent due to avascular, non-keratinized, no pigment, well organized uniform collagen, dehydration.  STRUCTURE + DEHYDRATION = CLARITY

• can visualize iris and choroid (through pupil), can't visualize ciliary body
• anterior uveal tract is iris and ciliary body
• anterior uveitis is inflammation of iris and ciliary body

• stroma is collagen and cells with only posterior epithelium, which continues over ciliary process and is contiguous with sensory retina and retina pigmented epithelium.  
• Has sphincter (pupil margin) and dilator (sun spokes) muscles (neuroectoderm from epithelial layer).  
• Color and shape varies
• anterior uvea, vascular tunic

• anterior uvea, vascular tunic
• two cell layers of retina and uveal tissue (muscles, vessels)
• iris posterior epithelium continues over ciliary body and blends into sensory retina and retinal epithelium
• functions: 1. neuroepithelial cells make aqueous humor.  2. muscles control aqueous humor outflow (drainage angle).  3. accomodation via muscles, near and far vision caused by changing tension on zonules/zonular ligaments
• (egg yolk in mushroom cap)

made by ciliary body neuroepithelial cells, flows through posterior chamber across lens and out pupil into anterior chamber, around chamber and out through trabecular meshwrok of iridocorneal/filtration angle (circumferentially deep to limbus at edges of anterior iris, not just sagittal!)

• posterior uvea/vascular tunic
• between sclera and retina
• tapetum is part of choroid
• vessels are orange-red and less regular and defined than retinal vessels
• function: blood supply nourishes and removes waste from outer portion of retina, lymphatic drainage.
• intrinsic nerve supply, secretory cells
• continuous with pia-arachnoid mater around optic nerve

capsule on outside is basement membrane of lens epithelial cells.  Anterior capsule thicker than posterior (with age) because anterior epithelium keeps dividing and migrating to equator (nuclear sclerosis - lens hardens and can't accomodate).  Posterior epithelial cells go away after development.

• develops from optic cup
• POR - pars optica retinae (sensory)
• PIR - pars iridica retinae (non-sensory, part of iris epithelium that is continuous)
• PCR - pars ciliaris retinae (non-sensory, part of ciliary epithelium that is continuous)
• pigmented epithelium lines outside and down the inside of the nerve
• 10 layers, Pigmented epithelium closest to sclera, 9 layers of photoreceptors including rods and cones between that and vitreous

• cranial nerve 2
• axons of retinal ganglia converge at optic disc, myelinate, exit through lamina cribosa in sclera.  Covered by meninges, pas through periorbita, though optic foramen.  Head (disc) visible in eye exam

• examining structures in back of eye (wall of the organ opposite the opening). 
• optic nerve, retina, choroid, tapetum, retinal vessels

• protect the globe and other structures
• sweep particles from ocular surface
• restrict tear film overflow from eye
• precorneal tear film (produce some of tear film, there are MANY glands in the eyelids)
• Lacrimal pump to assist drainage of the pre-corneal tear film

• medial to lateral
• start at 8-9d, done by 2-3wk
• premature - need lube!!!  No glands yet!!
• delayed - gentle opening with cotton and saline, flush and clean, fluorescein, tx PRN
• Neonatal ophthalmia (swollen eyes or lids pre-opening) is an EMERGENCY

• born with no eyelid in some place!  Congenital but may present at any time including never
• all species, more in some cat breeds
• hair is rubbing on globe (trichiasis) so usu need Rx.  Can cryo the hairs or lip-to-lid transposition (in cats, not horses)

• choristomas (normal skin in abnormal place)
• any species
• any ocular surface - lid, nictitans, cornea, lacrimating caruncle
• remove b/c irritating
• may not have visible hairs for months, often mean lid can't close properly, damage rest of eye.
• GOOD exam - what if it's full thickness?

• normal hairs touching ocular surface
• misdirected lashes vs normal facial hairs from entropion or nasal fold, etc.

• supernumerary cilia arising from tarsal or other gland openings to rub on the eye
• MOST COMMON
• normal hair growing from abnormal place.  
• Not all animals symptomatic, don't even need to tell O

• hairs growing through palpebral conjunctiva and touching cornea or conjunctiva
• common in Shih tzu, Lhasa, dogs
• VERY irritating, severe disease quickly!!.  VERY hard to find sometimes.
• May be able to see dark spots, but take a while to erupt so present in middle age?  Warn O.

• microcryoepilation: preferred! may cause eyelid depigmentation, possibly transient. Could also necrose so only a little area!
• Epilation/plucking: just one?  Clients may be able to do themselves.  No really advised. 
• Electroepilation: needle, current, smoke.  More than a few - scar!!
• excise: ectopic or single hairs only!  Biopsy punch
• divert offending hairs: turn lid margin away from cornea (entropion sx)
• DO NOT CUT LID MARGINS
• May want to refer.

• abnormally large palpebral fissure but otherwise normal lids and globe.  Lots of "scleral show".  Desirable in some breeds (St. Bernard, Bloodhound, Clumber spaniel), worrysome in brachycephalics
• tx: medial canthoplasty +/- lateral canthoplasty.  REFER

• rolling in or inward tilt of the eyelid margin toward cornea.  Okay as long as hairs don't CONTACT--it is never okay for hairs to rub the cornea
• congenital (most common in d/c) vs spastic (excessive squint due to ocular pain, self-perpetuating) vs cicatricial (scarring) vs secondary to enophthalmos.  
• Can therefore be primary or secondary (dehydrated, sick, stressed neonate foals, goats, lambs
• signs: epiphora, mucus, blepharospasm, conjunctivitis, corneal disease in adjacent cornea, self-trauma, ROLLING IN OF LID MARGIN (NEVER NORMAL)
• examine before and after anesthestic to reduce spastic so you don't remove too much/over-correct.  
• Sx: incise just where hairs start to grow, parallel lid margin length of entropion, roll eyelid out and take as much out ("tuck) as rolled. Take a slip of muscle too and closure is nicer. Suture in middle, and keep suturing middles until closed.  Can just tack if you think it's temporary, esp in LA. Wound clips! or SQ "bleb" next to eye (procaine penicillin), everts lid for 2-3 days

• congential vs cicatricial (scarring) vs transient seen in large dogs.
• signs: turned out lid, red eye, conjunctivitis
• tx: refer!  Not crucial, hairs not rubbing eye

• dog: sebaceous adenoma, papilloma, histiocytoma, melanoma
• cat: squamous cell carcinoma, fibrosarcoma
• horse: squamous cell carcinoma, sarcoid, melanoma
• cow: squamous cell carcinoma

• most common eyelid tumor in middle aged to older dogs
• looks like a papilloma or wart
• may cause eyelid inflammation if gland ruptures into tissues.
• Usually benign (usually more visible between head and tail)

• most common ocular tumor in horse, cow, (cat)
• variable presentation

• most common skin tumor in horses
• variable presentation

• NEED histo to diagnose (but careful with needles near the eye!)
• remove ASAP in horse, cow, cat (usu benign in dogs).  Also if looks inflamed or causing eye disease/inflame.  
• REMOVE BEFORE >1/4 lid length (refer after)
• assess regional lymph nodes--go on a tumor hunt before sx to get px

• simple excision, "V" or parallel lines with a "V" at the bottom (for larger, don't give eyelid away)
• close tarsal plate and skin using 5-0 or 6-0 vicryl.   NEVER CLOSE CONJUNCTIVA (suture rubs cornea
• Use buried figure 8 suture in tarsal plate to keep knot away from lid margin and conjunctiva.
• eyelid wounds bleed profusely but also heal really well
• just make sure you close the tarsal plate, and don't give away eyelid or skin if you can help it.

• Horner's
• space-occupying mass in orbit
• ANY condition causing enophthalmos (PAIN)
• phthisis bulbi or microphthalmos
• Idiopathic protrusion ("Haws" in cats?)
• Neoplasia of gland of nictitans
• TETANUS (spasmodic prolapse due to spasmodic globe retraction)

• Scrolling of cartilage: deformed tips of crossbar (refer)
• trauma: fine if small, refer if large (repair causes corneal ulcers)
• Inflammatory diseases: any conjunctival can cause, "atypically pannus", habronema in horses, granulomatous diseases in dogs
• neoplasia: SCC esp in LA, adenocarcinoma of gland, lymphoma
• follicular conjunctivitis: self limiting and cosmetic, increased mucoid d/c esp after swimming, look for follicle hypertrophy on everted nictitans, "puff"
• cherry eye: prolapse of gland, esp in dogs.  Refer large breeds and recurrent (cartilage deformity usu)
• Repair via Morgan Pocket Technique: incise on each side, make a pocket and leave holes on either end for drainage, make sure sutures don't rub cornea)

• it gets them. A lot.
• bulbar surface needs to be examined in every species with adjacent ulcer or delayed healing.
• ESP HORSE - they have a pocket on the bulbar surface
• Don't grab ON edge, just near
• a circular ulcer = infection because that's how bacteria grow

ARE BAD

• lacrimal gland, gland of the 3rd eyelid (conjunctival goblet cells, tarsal glands)
• lacrimal puncta
• canaliculus
• lacrimal sac
• nasolacrimal duct
• drain out the nose

• keeps corneal surface smooth and moist for comfort, clarity, transparency
• delivers nutrients to cornea and remove metabolites
• flushes debris and mucus from eye
• lubrication for smooth lid movement
• many other functions (immunoglobulins, enzymes, transport)

• quantitative: decreased aqueous layer shown by schirmer tear test = KCS
• qualititative: decreased mucin and/or lipid, aqueous can't do its job

• lacrimal gland
• ocular surface
• interconnecting innervation
• three portions inter-relate to control tear secretion and ALL are critical for ocular health
• assess quantity of tears, quality of tears (adhesion or evaporation) and assess related nerves (corneal sensation, assess lacrimal function)

• abnormal QUALITY of tear film due to poor adhesion or evaporation
• signs of dry eye in the face of a normal Schirmer - hard to dx.  Dx via tear film break up time (TFBUT) and tear analysis
• caused by chronic conjunctivitis, blepharitis.  Congenital?  Omega 3?

• schirmer
• fluorescene
• intra-ocular pressure

• reduced quantity of tears as seen by schirmer tear test.  One of most common SA ocular dzs. Chronic degenerative disease of cornea/conjunctiva, causes discomfort
• usu dogs, sometimes cats and horses (esp Burmese cats). rare in other species. 
• signs: discomfort, discharge (mucoid to mucopurulent).  CLASSIC: adherent filaments of mucus stuck to cornea, conjunctiva, lid.  Hard to remove. 
• can cause keratitis (haze, clouding, neovascularization, pigmentation  of cornea), corneal ulcers.  Neurogenic are accompanied by ipsilateral dry planum nasale, nostril and nasal passage (xeromycteria - dry nasal mucosa)
• Ear exams, esp for neurogenic, corneoconjunctival cytology and culture.  STT and fluroscein (watch for ulcers, can't heal!), cytology, culture
• Horses with KCS - endoscopy, skull rads, CT/MRI, thyroid assessment
• tx: correct inciting cause, tear replacement, increase tear production via immune moderation cyclosporine 0.2%, then 2%, then tacrolimus, MAYBE parasympathomimetics (pilocarpine, used in horses b/c their KCS usu neurogenic), control infection with abx, inflammation with NSAIDs or maybe steroids, eliminate mucus with acetylcysteine PRN.  If medical doesn't work, parotid duct transposition (great in 50%, un-do 20%)
• MOST IMPORTANT IS TO CONTROL LACRIMAL GLAND INFLAMMATION VIA IMMUNE MODULATORY DRUGS (CYCLOSPORINE OR TACROLIMUS) IN DOGS.  HORSES GET PILOCARPINE. 
• px: fair to poor dep on STT, maintain tx FOR LIFE so warn O.

• Autoimmune (most dogs): T-cell mediated lacrimal gland adenitis
• drug-induced/toxins: parasympatolytic (atropine), tranquilizers/anesthetics, sulfa drugs, etodolac, locoweed
• LA - gutteral pouch disease: damage to parasympathetic innervation to glands
• Neoplasia of gland
• THO (temporohyoid osteoarthropathy)

• both cause red vessels around eye.  
• hyperemia is and ocular SURFACE disease, vessels move when you tug on the conjuntiva via the eyelid
• injection has bigger vessels with less branching, and don't really move when you touch the eyelid.  Deeper - corneal or inside.

• conjunctival hyperemia (puff and fill with edema)
• chemosis
• ocular discharge (upset goblet cells increase production of mucin)
• hemorrhage
• follicles
• pruritus (scratching, leads to...)
• ulceration

• infectious (uncommon)
• staph aureus, staphy epidermidis, strep
• distemper
• herpesvirus
• calicivirus

• Non-infectious (MOST)
• allergic (often atopic)
• follicular conjunctivitis
• KCS

• FHV-1: stress (latency), MOST COMMON.  Dendritic ulcers, rhinitis, symblepharon (conjunctiva stuck to cornea)
• Chlamydophila felis: bilateral, chemosis, mild rhinitis, fever, enlarged submandibular LN, long term c/s.
• mycoplasma: chemosis, uni or bilateral, ocular  and nasal d/c
• feline eosinophilic keratoconjunctivitis: multifocal raised pink/pale white plaques, +/- ulcer.  Affects cornea, conjunctiva and 3rd eyelid.  65% also have herpes
• lipogranulomatous conjunctivitis: blepharitis, nodular conjunctivits, upper lid of white cats

• equine herpes virus: URI! 
• Moraxella spp: rare
• chlamydophila abortus
• chlamydophila pneumoniae
• parasites: onchocerca cervicalis, habronema spp, Draschia megastoma, thelazia

• bovine malignant catarrhal fever: HIGH mortality.  Alcephaline herpesvirus vs ovine herpesvirus
• infectious bovine keratoconjunctivitis: moraxella bovis
• Infectious Bovine Rhinotracheitis: Bovine herpesvirus I
• Chlamydophila abortus
• chlamydophila pecorum
• Parasites: thelazia, Oestrus ovis in sheep

• non-neoplastic
• dermoids (normal tissue)
• subconjuntival fat prolapse
• granulation tissue
• cysts

• neoplastic
• squamous cell carcinoma (most common in all but dogs)
• hemangioma and hemangiosarcoma (NBD in conjunctiva, doesn't spread)
• papilloma/histiocytoma
• mastocytoma
• lymphoma
• melanoma (usu malignant in cats and horses)

• virus: cidofovir, famciclovir, lysine
• bacteria: doxycycline, topical tetracyclines or erythromycin, ciprofloxacin
• immune: (feline eosinophilic keratoconjunctivitis) topical cyclosporine, topical steroids, +/- antivirals?
• sx: (lipogranulomatous, neoplasia/mass) full removal vs debulk vs exteneration of eyeball
• parasitic: remove parasite, ivermectins

• detects and evaluates corneal ulcers: hydrophobic corneal epithelium and descemet's membrane repel, hydrophilic stroma binds.  Can use cobalt filter or UV light to excite
• seidel test: leaking aqueous humor. CONCENTRATED fluroescein (dark orange, not fluorescent), streams bright green when diluted by aqueous humor, will fluoresce
• determines nasolacrimal patency

• vascularization
• result of chronic inflammation (superficial vs deep tells you where)
• superficial: brighter red, fine, branches, cross limbus, "tree"-like, from conjunctival vessels, suggest superficial corneal or external eye disease like chronic keratitis
• deep: darker, shorter, straighter with few or no branches, do not cross limbus, "hedge"-like.  From perilimbal ciliary vessels, suggest deep corneal or intraocular disease like glaucoma, uveitis, corneal stromal abscess

• edema
• "ground glass" or "fluffy" appearance
• epithelial or endothelial disease.
• Epithelial: ulcers = loss of barrier function.  Focal edema, often mild.  Fluorescein +
• Endothelial: primary or secondary dysfunction of active ion pumps with loss of barrier function.  Diffuse edema, can be marked.  Fluorescein -.  

• pigment
• intra- or extracellular melanin deposition.
• Epithelial/stromal: chronic inflammation
• Endothelial: congenital anomalies, deflated iris cysts or anterior synechiae
• Cats with corneal sequestrum can also have brown or black but it isn't pigment.  

• inflammatory cells - leukocytes in corneal stroma or epithelium.  Often mucusy or creamy.
• diffuse or focal with stroma abscess formation
• usually indicate corneal infection or foreign body, often an emergency!!

• keratic precipitates
• plaques of inflammatory cells ADHERENT to corneal endothelium.  Usually on ventral endothelium
• indicates prior or current anterior uveitis

• scar tissue
• flat, dull, white or grey color tone, often indistinct borders
• results from corneal fibrosis and disorganization of stromal collagen
• secondary to any corneal insult or injury (nonspecific)

• deposition of lipid/mineral.  Refractile, appears "sparkly", well-defined.  
• Calicum or cholesterol most common
• primary: inherited corneal dystrophies (irregular metabolism in cornea)
• secondary: corneal degeneration (inflammation), systemic diseases (increase blood lipid or mineral levels)

• superficial: brighter red, fine, branches, cross limbus, "tree"-like, from conjunctival vessels, suggest superficial corneal or external eye disease like chronic keratitis
• deep: darker, shorter, straighter with few or no branches, do not cross limbus, "hedge"-like.  From perilimbal ciliary vessels, suggest deep corneal or intraocular disease like glaucoma, uveitis, corneal stromal abscess

• epithelial loss only, acute
• distinct epithelial borders cause distinct fluorescein outline.  
• Minimal inflammation
• heal in days

• epithelial loss only, chronic, with non-adherent epithelial "lip" (loose flaps). epithelial basement membrane or stromal abnormality a possibility.  ONLY IN DOGS (cats and horses have viral and fungal similar things)
• indistinct fluorescein halo around border (pathognomonic)
• minimal inflammation, variable corneal vascularization
• heals in days

• epithelial and stromal loss, acute or chronic
• fluroescein stains walls and floor, have "depth"
• frequently inflammation of cornea and anterior chamber
• heal in weeks to months

• complete stromal and epithelial loss, acute or chronic
• floor does not stain, but walls do (watch for pooling)
• corneal and anterior chamber frequently inflamed
• floor is very clear and may bubble out - glass bottom boat!  NEVER POP A BUBBLE
• heal in weeks to months

• full-thickness stromal and epithelial and endothelial loss, aqueous humor may leak out.
• Fluorescein sticks to walls but not floor, floor very clear (because nothing is there). Fibrin clot (looks like mucus) or iris (iris-colored mass) may fill defect in cornea.  May be dyscoria/pulled pupil, anterior chamber may be shallow or absent and cornea may wrinkle.  Hyphema (uveal hemorrhage from rapid pressure change).
• heal in weeks to months

• chronic healed ulcer with intact epithelium
• fluorescein may pool in dip but will wash away.
• Thinned cornea, minimal inflammation though previous scarring, vascularization or pigment may remain. 
• Just there to be confusing

• superficial ulcers
• find and remove the inciting cause
• prevent secondary infection via topical abx
• prevent/treat reflex uveitis with atropine +/- systemic NSAID
• prevent self-trauma with ecollar
• recheck on 7-10 days (should be HEALED)
• NEVER: topical corticosteroids or topical anesthetics FOR ANY ULCER, NSAIDs only in emergencies

• indolent ulcers (only occur in DOGS for tx purposes, viral or fungal in cats and horses and this makes it worse)
• debride loose epithelium with dry cotton-tipped swab
• prevent secondary infection
• prevent/treat reflex uveitis with atropine +/- systemic NSAIDs
• prevent self-trauma with ecollar
• may require grid keratotomy, punctate keratotomy, diamond burr debridement, contact lens, keratectomy
• NEVER: topical corticosteroids or topical anesthetics FOR ANY ULCER, NSAIDs only in emergencies

• topical anesthetic and sedation
• debride all loose epithelium (indolent ulcer)
• 25g needle
• score stroma in grid pattern
• DOGS ONLY, 90% heal after this

• stromal, descemetocele, perforations
• Pretty much is or has been infected. Need prompt tx!
• diagnostics: exam with STT, fluorescein but NOT tonometry, culture, cytology, gram stain (swab the broder not the floor)
• find and remove inciting cause
• topical antimicrobials based on cytology, q2-4h (Solutions only, don't touch the eye!), atropine, e-collar, monitor!  
• Maybe: Systemic NSAIDs for analgesia and uveitis, anticollagenase to prevent active melting, EVERY 2 HOURS (acetylcysteine, EDTA, tetracyclines, serum)
• NEVER: topical corticosteroids or topical anesthetics FOR ANY ULCER, NSAIDs only in emergency
• Sx: only for rapid progression, deep or perforated.  Conjunctival grafts or corneal grafts to "seal" and provide blood supply (not third eyelid flap or tarsorrhaphy, just hides doesn't help)

• inciting cause still present
• infected
• indolent ulcer

• infiltrates (appear yellow or green) in cornea
• corneal edema
• corneal melting (keratomalacia) due to enzymatic digestion from proteases from MO, leukocyte and epithelial cells.  Looks gelatinous and may have anterior displacement
• uveitis out of proportion, more than seen in superficial ulcers
• stromal loss (infection is the only reason they get deeper)
• most show ALL these signs

• find and remove the inciting cause
• diagnose and treat the infection

• brown/black discoloration in feline corneal stroma.  May be surrounded by ring of ulceration, +/- vascularization.  +/- painful, usu unilateral and central.  Esp brachycephalic
• non-specific response to keratitis?  Stromal necrosis, not sure why.
• medical tx: if not painful, resolve chronic keratitis, topical abx, antivirals and/or lubricants, it may slough in several months (or may not)
• surgical tx: superficial keratectomy for painful.  Conjunctival or corneal grafts needed for deep sequestrum to fill defect, may prevent recurrence

• most common in cat (though appear in others).  FHV-1 MOST COMMON cause of all conjunctivitis, keratitis and corneal ulceration in cats.
• punctate corneal ulcers are earliest, dendritic are pathognomonic for FHV (coalesce to form geographic)
• dx: cytology (inclusions rare, rest non-specific), IFA not good, serology doesn't help since everyone has it, virus isolation is time-consuming, expensive and still false +.  PCR is sensitivit/specific but not everyone is symptomatic.  JUST DO TX, don't do tests
• tx: prevent secondary bacterial, prevent/tx reflex uveitis, topical antivirals (cidofovir BID), lysine MIGHT prevent recurrence? Oral famciclovir. Tx all immunosuppressive conditions but avoid immunosuppressive meds and stress. DON'T DO GRID KERATOTOMY

• aspergillus, fusarium and candida
• predisposing: topical steroids, abx, corneal trauma, corneal FB.
• Signs look like any ulcers
• CLINICAL FINDINGS: white, gray, yellow, brown or black corneal plaque, fluffy or feathery appearance to lesion, satellite lesions, deep stromal abscess (usu fungal in horse)
• dx with corneal swab, scraping or biopsy (last two preferred).  Cytology least sensitive, histopath great but hard to get sample, culture most sensitive but too slow, PCR high SE low Sp from environment, in vivo confocal microscopy is the best but limited availability
• medical tx: prevent/tx secondary bacterial, prevent/tx reflex uveitis (balance systemic NSAID with inhibition of corneal vascularization), topical antifungals, manual debridement, systemic antifungals?  MONTHS OF THERAPY
• surgical tx: don't respond to medical or rapid progression.  Keratectomy to remove plaques, conjunctival grafts for blood supply and support, or keratoplasty to replace lost tissue

• medical for <50% stromal thickness, topical and systemic abx, atropine, systemic NSAIDs.  Prevent additional self-trauma
• sx for >50% stromal thickness.  Replace/remove iris if prolapsed, suture corneal defect, refill anterior chamber, +/- corneal grafts for large, +/- lens removal if capsule compromised

• superficial removed with eyewash, Q-tip, fine forceps
• deep need keratectomy
• after removal, topical abx, atropine, monitor for infection.  Systemic anti-MO if penetrated anterior chamber
• Deep can be pushed deeper, be careful and refer!
• post-removal infections handled like deep ulcers

• appearance: corneal ingrowth of blood vessels, superficial white nodules or plaques, faint fluorescein staining? Focal or diffuse, unilateral or bilateral
• diagnosis: clinical appearance and corneal cytology (ANY eosinophils present with other inflammatory cells)
• Treatment: topical steroids and/or topical cyclopsorine.  Topical antiviral?  DON'T use systemic megestrol acetate (historical, bad effects)
• Often controlled, not cured

• dogs only
• immune-mediated disease of unknown cause (UV and genetics, GSD, shepherd crosses, greyhounds), infiltrate of plasma cells, lymphocytes, blood vessels and pigment
• appearance: lateral cornea over corneal surface, red "fleshy" plaque  (+/- pigment, "cobblestone"), may be on nictitans or conjunctiva too.  Bilateral and symmetric. Non-painful, not ulcerated
• ATYPICAL CSK/Pannus occurs on nictitans
• Dx: appearance, breed, can cytology/histopath
• tx: controlled, not cured.  Topical cyclosporine/tacrolimus, topical steroid (start with both, taper off steroid), UV light avoidance (doggles!).  Lifelong tx.

• pigment is a non-specific response to chronic keratitis, some dogs/breeds have more (pug, peke, shih tzu, boston, from nasal trichiasis, entropion, folds, KCS, lagopthlamos/incomplete blink etc)
• thick plaque of pigment that causes blindness without tx, takes a long time to go away.  Begins at nasal cornea and spreads, usu vascularization.
• dx: via appearance
• tx: correct primary problems (cyclosporine for KCS, surgical correction of face to stop irritation), then palliative (lubricants, topical cyclosporine/steroids, beta-irradiation for severe?  NO KERATECTOMY)

• primary: rare, papilloma (young), SCC, hemangioma/HSA. Dermoids are NOT a neoplasm
• secondary: more common (extensions from adjacent).  SCC and HSA most common.
• Metastatic: rare, lymphoma (salmon/pink to white corneal infiltrate. Ocular = stage 5, it's EVERYWHERE

• granulation tissue: red, opaque, smooth, raised masses on cornea, highly vascular. Secondary to chronic keratitis
• corneal epithelial inclusion cysts: raised or flat, solitary, white to pink masses, nonpainful, chronic, unlateral.  From traumatic/surgical seeding of epithelial cells to deeper cornea (no MO or leukocytes on cytology)

• dystrophy: lipid deposition in corneal from familial metabolic abnormality. Bilateral and symmetrical, central cornea, any layer, elliptical/racetrack, non-painful, no therapy.  Husky, CKCS, Bichon
• degeneration: lipid or mineral deposition secondary to primary corneal disease. Unilateral, vascularization, any part of cornea, usu epithelial/subepithelial. Can cause non-healing ulcers.  Chelation therapy if painful - bind mineral in tears.  May also be caused by systemic like hyperlipidemia/phosphate/Ca, DM, hypothyroid, hyperadrenocorticism, pancreatitis, hyperparathyroid, lymphoma

• dystrophy: heritable, corneal edema in older, usu lateral first, boston, chi, dach.  Tx with topical hyperosmotic to slow, keratectomy and conjunctival advancement hood flap. 
• degeneration: secondary causing edema (uveitis, glaucoma, anterior lens luxation, intraocular sx), tx underlying cause!  Hyperosmotics may be palliative.

uveitis, glaucoma, anterior lens luxation, intraocular surgery

• benign canine primary scleral neoplasms from perilimbar melanocytes within sclera.  
• Young dogs (2-4y): invasive, rapid growth
• older dogs (8-11y): stationary, usually incidental.
• Esp in golden, lab and GSD.

• dorsolateral quadrant first, smooth black mass, may invade cornea
• tx: monitor older dogs (NBD).  Enlarging masses - make sure dx is right (not scleral extension of intraocular neoplasm).  Surgical excision, cryotherapy, beta irradiation, and/or laser photocoagulation

• middle vascular layer
• iris: stroma, contrictor pupillae (sphincter, PNS), anterior epithelium and dilator pupillae (SNS), posterior pigmented epithelium. Control pupil size/light, increase depth of field for near (miosis)
• ciliary body: posterior to iris, pars plicata (ciliary processes), pars plana. Epithelial cells - inner non-pigmented, outer pigmented.  Stroma. Produce aqueous humor, accomodation, increases drainage of aqueous humor
• choroid: posterior uvea, CT, vessels, pigmented cells, tapetum (fibrous in herbivores, cellular in carnivores).  Horses have stars of Winslow. 
• tight jctns make barrier, fluid in eye is ultrafiltrate of blood with no proteins or cells.

homozygous merle, autosomal recessive.  Iris hypoplasia (poorly developed), corectopia (misplaced pupil), iris coloboma (sector defect in iris), microphthalmia, cataracts, equatorial staphylomas, scleral/retinal defects, optic nerve coloboma

incidental, congenital, incomplete resorption of embryologic vascular structure and mesenchymal tissues.  Usually iris to iris, can be iris to lens or cornea (dysplastic)

• congenital. clear (usu), pigmented or filled with blood
• congenital or acquired
• goldens, great dane, bostons

congenital. normal vs merle ocular dysgenesis, could come with iris coloboma or hypoplasia.  Congenital deafness in some animals

flat lesion, congenital, doesn't change over time, could become diffuse iris melanoma.  Freckles.

• degenerative/acquired
• progressive thinning of stroma, associated with chronic uveitis, glaucoma, age or trauma
• can cause weak sphincter = abnormal PLR

• exogenous (trauma, ulceration = reflex, etc) vs endogenous (systemic illness etc)
• ocular pain, corneal edema, episcleral injection or ciliary flush, miosis, aqueous flare (increased turbidity of aqueous humor due to proteins from breakdown of blood barrier from inflammation, PATHOGNOMONIC)
• anterior, posterior or pan
• aqueous flare (hypopion, hyphemia), keratic precipitates, decreased IOP, retinal detachment.  Can cause synechia, phthsis bulbi (shrivel), cataract, lens luxation, virtreal degeneration, hyperpigmented iris, corneal edema. 
• Caused by all the things
• tx: primary cause, topical anti-inflamm (NSAID vs steriod), systemic anti-inflamm, systemic immunosuppressives, mydriatics (atropine for pain, stabilization).

• common intraocular neoplasm, can become malignant melanoma.  Dark moving across eye?
• tx with local resection vs enucleation vs exenteration

• usually malignant, can metastasize
• cats
• remove pre-scleral involvement!  
• causes uveitis, glaucoma, hyphema
• 75% metastasize before enucleation
• reasonable prognosis for survival

• slow or rapid color change of eye with raised pigment, pigmented cells floating around.  Irregular pupil?
• dyscoria, glaucoma, metastasis, uveitis
• tx: enucleation

• dogs
• adenoma vs adenocarcinoma, less malignant in eye than rest of body.  
• Tx: removal of mass vs enucleation
• Unlikely to metastasize, good prognosis for life

• dogs and cats
• MOST COMMON SECONDARY INTRAOCULAR TUMOR
• often associated with FeLV in cats

• lenticular sclerosis: epithelial structure within a capsule, so new cells produced but desquamation not possible.  Central lens fibers become compressed, more dense, less transparent. Bluish-grey haze but no vision loss, fundus VISIBLE THROUGH LENS.  Pupil margin more noticeable.
• cataract: any opacity of lens or capsules.  May interfere with vision, FUNDUS NOT VISIBLE through.

• incipient: 10-15% of lens affected, tapetal reflection still visible (around), earliest cataract you can see, does not really interfere with vision
• immature: anything between incipient and mature. tapetal reflection still visible, variable vision.
• mature: tapetal reflection gone.  Eye is blind.  Leukokoria = white pupil
• hypermature: lens resorption (decreased volume with same area of capsule, wrinkle, anterior chamber deeper, tapetal and vision may return, "sparkly". 

• intumescent (immature or mature): lens "swollen", absorbs aqueous humor, shallow anterior chamber, SPLITS at suture regions
• morgagnian (hypermature): lens nucleus sinks to bottom of liquified cortex

• inherited in dogs.  Metabolic from DM common in dog too. 
• chronic uveitis in cats/horses
• nutrition in puppies/kittens from milk replacer

• extent of visual defect (no vision loss means nothing to gain!!)
• general health
• condition of eye
• client commitment (medication for MONTHS)
• animal temperment (medication for MONTHS)

• complete displacement of lens from patellar fossa. Anterior or posterior (side to side is subluxation).  Due to loss of zonular ligament support.
• Primary etiology: inherited causing abnormal degeneration - Jack russels
• secondary: chronic uveitis (cats), trauma (rare, needs massive force), chronic glaucoma (enlargement of globe - chronic stretch of ligaments), hypermature cataracts (contraction of lens capsule)
• Signs: aphakic crescent (suddenly see around lens), iridodonesis (agitated mvmt of iris with eye mvmt), phacodonesis (lens), vitreal prolapse, corneal edema, shallow or deep anterior chamber, cataract, uveitis, glaucoma, retinal detachment

presence of artifical intraocular lens post-sx

absense of lens, congenital or post-sx

small lens

conical protrusion of lens

spherical protrusion of lens

nervous and vascular and lymphatic systems

• epithelial and neural tissues
• conjunctivitis with mucoid to mucopurulent discharge
• lacrimal adenitis (reduced tears, acute KCS)
• keratitis, corneal ulceration
• multifocal chorioretinitis
• optic neuritis

• corneal edema ("blue eye" in puppies)
• anterior uveitis

• conjunctivitis
• anterior uveitis
• pars planitis
• lens luxation
• retinopathy (multifocal thinning and hemorrhage)
• uveal lymphoma

• Retinal dysplasia
• uveitis
• uveal lymphoma
• spastic pupil syndrome (alternating dilation and constriction due to inflammation of autonomic ganglia, precursor to lymphoma, poor px)

• disseminated pyogranulomatous vaculitis, more common with dry form
• anterior uveitis
• hyphema
• chorioretinitis
• retinal hemorrhage
• retinal detachment
• retinal perivascular exudates (vessels cuffed in white fluffy-ness)
• optic neuritis

• ocular: ulcerative conjunctivitis
• systemic: URI, oral ulceration, +/- polyarthritis

• initial = URI, conjunctivitis, limited keratitis
• can cause chronic, recurrent ocular disease (conjunctivitis and keratitis)
• corneal sequestrum
• eosinophilic keratitis
• stromal keratitis
• KCS
• uveitis

• retinal dysplasia
• usu + cerebellar hypoplasia

• pedunculated cauliflower-like masses on eyelid, conjunctiva, cornea.  
• Self-limiting, otherwise healthy

• blepharitis
• orbital abscess/cellulitis
• conjunctivitis
• keratitis
• granulomatous anterior uveitis and chorioretinitis
• retinal detachment
• optic neuritis

• anterior uveitis
• chorioretinitis
• endophthalmitis
• +/- intraocular hemorrhage
• often unilateral (MAKES NO SENSE). Zoonotic

• anterior uveitis, hyphema, retinal hemorrhages, chorioretinitis, optic neuritis
• lesions due to thrombocytopenia, vasculitis, hyperviscosity

• conjunctivitis
• anterior uveitis
• corneal edema
• retinal hemorrhages
• chorioretinitis
• retinal detachment (direct or indirect)
• uveal hemorrage (indirect, glomerulo-nephritis and hypertension)

• anterior uveitis
• chorioretinitis
• extraocular myositis
• scleritis
• vitritis
• optic neuritis

• immune-mediated disorder targeting melanocytes (eyes and skin in dogs)
• ocular: anterior and posterior uveitis, uveal depigmentation, retinal detachment
• dermatologic: poliosis (whitening of hair) and vitiligo (skin depigmentation)

• hypertension
• thrombocytopenia/coagulopathies (rodenticide)
• hyperviscosity syndrome
• anemia
• diabetes mellitus

• initial lesion in area centralis, mirror image, line connecting the two, progressing to generalized retinal degenration
• caused by taurine deficiency (with DCM) in cats.

• lymphoma - MOST COMMON IN DOGS AND CATS
• HSA
• osteosarc
• malignant melanoma
• mammary and pancreatic adenocarcinoma
• mast cell tumors
• SCC
• transitional cell carcinoma

• sulfa antimicrobials
• etodolac/acetominophen

• define clinical problem specifically for the P
• assess the cause
• formulate specific objectives of therapy - medical, surgical
• Consider options: medical vs surgical
• educate clients: benefits and limitations of tx, prognosis for life/function/cosmetic, short and long term cost
• assess therapeutic effect (reasons for failures)
• surveillance for local/systemic side effects

• topical: eyelid, cornea, conjunctiva (+/- iris, ciliary body)
• subconjunctival: cornea, iris, ciliary body, anterior chamber (+/- choroid, retina)
• retrobulbar: NOT INDICATED
• intracameral (anterior chamber)/intravitreal (vitreous) 
• systemic: eyelids, orbit, uvea, retina, optic nerve, anterior and posterior chambers, and vitreous

topical, systemic

• solutions/suspensions: short contact time, high application frequency, drug solubility limitations, stability
• ointments: longer contact time, lower application frequency, could worsen discharge

specific

• prevent infection: abx
• prevent/treat anterior uveitis: atropine

• prevent infection: abx
• prevent/treat anterior uveitis: atropine
• remove nonadherent epithelium: Q-Tip debridement
• encourage epithelial adhesion: punctate/grid keratotomy +/- tarsorrhaphy +/- nictitans flap

• prevent infection: abx
• preserve pupil/pan relief: atropine
• wound support: cyanoacrylate adhesive (glue), conjunctival flap (NOT nictitans flap)

• treat presumed infection: intensive abx
• prevent/treat stromal "melting": abx, anticollagenase drugs
• treat anterior uveitis: atropine
• support weakened cornea: conjunctival flap

• treat cause: abx, steroids
• reduce chemosis (edema): topical hyperosmotic

• stimulate lacrimation: topical cyclosporine/tacrolimus
• replace tears: artificial tears
• treat infection: abx (intermittant)
• reduce corneal, conjunctival inflammation: steroids (intermittant)
• reduce discharge: hygiene

• reduce inflammation: steroids, NSAIDs, atropine
• tx infection (bacterial, rickettsial, mycotic etc): abx etc PRN
• preserve pupil: atropine, phenylephrine
• prevent/treat secondary glaucoma: CAIs, beta-blockers, +/- prostanoids

• reduce vitreous volume: oral/IV osmotics
• decrease aqueous production: CAIs, beta-blockers, prostanoids, cyclocryosurgery, laser cycloablation
• increase aqueous outflow: prostanoids, surgery
• prevent glaucoma in fellow eye: lifetime prophylaxis with topical CAI, +/- beta blocker

• decrease aqueous production: CAIs, beta-blocker
• decrease inflammation if present: NSAIDs +/- steroids
• decrease vitreous volume: osmotic agents
• decrease fibrin: TPA into anterior chamber

• treat infection: abx
• relieve inflammation/swelling: anti-inflammatories, perioral drainage
• eliminate inciting cause: check teeth, sinuses, r/o FB

• decrease inflammation: NSAIDs, systemic steroids
• prevent/treat infection: +/- abx, +/- antifungals (systemic)

• treat primary cause: reduce choroiditis (NSAIDs, steroid), reduce hypertension (diruetics, antihypertensive drugs), tx infections (abx, antifungal)
• encourage reattachment: duretics, tranquilizers, corticosteroids, all have ?

group of ocular diseases that cause high intra-ocular pressure causing optic nerve and retinal disfunction, causing loss of some or all vision

• production: active secretion (80-90%), small amt of diffusion, ultrafiltration (pressure sensitive)
• 1-1.5% of anterior chamber volume / minute
• conventional pathway - outflow: from CB through posterior chamber, pupil, anterior chamber, iridocorneal angle. 
• unconventional pathway - outflow: leaks out through uvea and into sclera, resorbed by conjunctiva etc.  Some goes into vitreous and cornea, but negligible.
• glaucoma usually due to outflow problem

• primary: iridocorneal angle (closed angle*, open angle, narrow, dysgensis) vs congenital (rare)
• secondary: uveitis, intraocular neoplasm, hyphema, lens luxation, intumescent (swelling) cataract, post-sx

• red eye - episcleral vessels (not conjunctival), so dark, thick, not branching. Cats don't get this
• lens luxation
• haab's stria (stretch marks) on descemet's membrane (aphacik crescent)

• the old one - weights, have to use the chart.  Not user friendly
• inexpensive and reasonably accurate?
• can't use in small corneas, cornea has to be horizontal, needs topical anesthesia, hard to use with low IOP

• reliable, simple, low maintenance cost, but expensive at first, topical anesthesia and a bit of a learning curve
• the pen you just tap to the eye
• recommended for GP
• gives a standard deviation so you know how accurate the reading is

• No topical anesthesia needed!  Calibrated for dif species, okay in small corneas, reliable
• but expensive and high maintenance costs
• require vertical cornea
• has probe that taps onto eye, can shoot off if not close enough

• dogs 16.7
• cats 19.7
• horse 23-39
• hawk 20.6

"cupped" ocular nerve--darker, has a halo around it.  Vessels dive in, don't show on surface like they normally do

• prostaglandin F2alpha: increase unconventional pathway outflow, increase conventional outflow, can decrease 30-40mmHg in an hour!  BID. Not good with lens luxation as causes miosis, darkens eyelashes and skin (Latanoprost)
• hyperosmotic: dehydrates everything, mannitol.  Short term but fast, opens iridocorneal angle. Good for pre-op lens luxation.  No good for uveitis (blood barrier not intact?)
• carbonic anhydrase inhibitors: no water goes into eye.  Topical rather than systemic. Dorzolamide TID. Increases retinal and ciliary blood flow so protective.
• beta-blockers: timolol, decreases production of aqueous humor, don't use with ulcers (toxic to epithelium)

• in primary you need to treat the second eye prophylactically
• in secondary you obviously treat the primary cause.

• meds not working?  
• Acute primary: cyclodestruction (CB destruction - inject gentamicin and dexamethasone), Gonioimplant to help drain. 
• acute secondary: enucleation, evisceration/prosthesis, cyclodestruction?
• chronic: enucleation, evisceration/prosthesis, cyclodestruction?
• Decrease production by killing CB or increase outflow with a shunt (hydrostatic) that releases outside sclera
• Avoid prosthesis in cats or cancer

• Minimal debridement
• perfect apposition of lid margin with figure 8 suture pattern

• Px: vision - guarded to poor.  Globe retention poor if ruptured, three or more muscles torn, hyphema, facial fractures, O unable to tx 
• complications: lateral strabismus, KCS, corneal ulceration, glaucoma, phthisis bulbi, eventual need for enucleation
• tx: enucleate or replace globe with temporary tarsorrhaphy (horizontal mattress), when in doubt replace. Oral and topical abx, systemic NSAIDs, ecollar

• Signs: depth!  Reflex uveitis, WBC infiltration, keratomalacia/melting.
• tx: REFER with ecollar! Surgical (conjunctival graft) for >50%, Medical if <50% (abx DROPS, pain control/atropine, systemic NSAIDs, topical antiprotease/anticollaginase, ecollar

• Clinical signs: (same) aqueous flare, miosis, iridal color change, keratic precipitates. Hyphema (blood in anterior chamber)
• ddx: (hyphema = uveitis) coagulopathy (hyphema),
•   LOCAL: trauma, primary neoplasia (rare), immune-mediated
•   SYSTEMIC: anything that causes vasculitis - neoplasia, immune-mediated, infectious, idiopathic (50%)

• Cocker spaniel
• basset hound
• beagles
• siberian husky
• shar pei
• chow

Small terriers (rat terrier, Manchester, jack Russell)

• Topical: prostaglandin analogues (latanoprost for dogs), carbonic anhydride inhibitors (dorzolamide), beta blockers (timilol)
• IV or oral osmotics: mannitol (IV), glycerol (PO), stopgap
• Anterior chamber paracentesis: stopgap
• sx: chemical cycloablation (IV gentamicin to kill everything, evisceration and prosthesis, enucleation

• Tx underlying cause
• anti-inflammatory corticosteroids if no ulcer
• control cycloplesia with atropine unless glaucoma
• +/- glaucoma meds PRN (dorzolamide)
• systemic therapy (anti-inflammatories or doxy?)

• Pressure-reducing meds: dorzolamide (NOT LATANOPROST) topically, methazolamide PO if needed, Mannitol IV if needed
• REFER for IntraCapsular LensEctomy (ICLE)
• tx uveitis in cats

• Amaurosis: 
• Ddx: Retrobulbar optic neuritis, central blindness/neuro, SARDS
• dx: electroretinogram shows retinal function (+ = neuro, - = SARDS)

• abnormal fundus
• ddx: opaque media, glaucoma, retinal detachment, optic nerve papilloedema, optic neuritis
• dx: SO MANY THINGS

• Infected ulcers
• penetrating or perforating corneal FB
• corneal lacerations
• anterior lens luxation

• rapid horizontal nystagmus persisting throughout life in Holsteins and Guernseys
• asymptomatic happy cows
• familial

Lymphosarcoma

• Exopthalmos without pain or fever in adult dairy cattle!!!  
• Rapidly or slowly progressive, unilateral or bilateral +/- lymphadenopathy
• usu older, BLV positive
• COMMON LOCATIONS: Orbit, abomasum, spinal cord, uterus, R atrium
• dx: CBC, BLV test, cytology of orbit aspirate (LYMPHOCYTES = DX)
• tx: salvage procedure to wait for calving - permanent tarsorrhaphy

Retropulse to r/o space-occupying mass like LSA

• Most common tumor of globe in cows, causes 10% of carcass contaminations
• signalment: middle-aged to older (7-9y), cows with little periocular pigmentation.  UV and irritants are risk factors, also viruses
• common sites: nictitans, temporal limbus, lid margins
• behavior: locally aggressive, rarely metastatic

• most common tumor of GLOBE in horses (sarcoidosis is most common skin)
• Signalment: middle aged to older, lightly pigmented coat/ocular areas, BELGIANS, HAFLINGERS, APPALOOSA and any CHESTNUT
• Risk factors: solar radiation (geographic location), chronic inflammation/irritation, loss of pigment in temporal perilimbal conjunctiva (onchocerca sp)
• most common sites: nictitans, temporal limbus, lid margins

• Cauliflower-like mass on nictitans or temporal limbus
• VERY variable (smooth, gelatinous, scaly, flat, discoid, exudative like fungal keratitis, often cheesy-looking).  Mimics other disease, ALWAYS keep SCC in mind
• can involve lids, nictitans, caruncle, conjunctiva, cornea or combinations
• THINK OF WITH ANY CHRONIC OCULAR LESION
• never forget to check the penis

• Dx: clinical appearance/exam, BIOPSY AND HISTOPATH (not cytology, looks like reactive epithelium)
• prognosis: directly proportional to SIZE, age, etc.  Histo very important!  Local recurrence common, but you can buy years and repeat as needed. RADIATION as cleanup helps a lot!!
• small lesions on nictitans or globe are fair/good, lid always guarded.  Large, ulcerated and all caruncle is poor
• REMOVE ASAM

• pre-op NSAIDs, broad-spectrum topical abx, atropine
• local excision (IMMEDIATELY)
• follow with Sr90 (best, radiation for LA), cryo or mitomycin or radiofrequency hyperthermia (may do nothing or hurt)
• enucleation if inoperable
• follow with radiation (Sr90), SCC is VERY radiosensitive but only penetrates ~1mm (clean-up, will delay healing)

• Most common skin tumor of horse, VERY common in eyelid, esp medial aspect of superior
• tx: cryo, BCG, ALDARA (?), xxterra not near eyes

• Granulomatous reaction to L3 larvae of habronema (majus and muscae) and draschia megastoma deposited in moist tissue (WOUNDS! medial canthus, urethral orifice, lacrimal caruncle, nasolacrimal duct) by flies (house and stable)
• Signs: eye or skin inflammation with ulcerative lesions containing SULPHER BODIES (moist areas with yellow caseious hard gritty concretions).  Inflammation erodes skin away!!
• derm disease, affects equine eye in warm climates (and NY)any age (often young to middle)common in ARABS AND LIGHTER COAT COLORS
• don't forget to look at the penis!

• dx: presentation, lesions, season. Granulomatous reaction with eosin, mast, collagenolysis (~50% will find larvae, rare to find on cytology)
• tx: REMOVE all granules and necrotic tissue, deworm, NSAIDs, topical steroids if cornea healthy.  Control flies, remove manure, PRAY for cold weather.  Catheterize nasolacrimal ducts if needed, may retain patency

• Horses.
• follicular keratoconjunctivitis, temporal limbal vitiligo (loss of pigment at lateral limbus of iris).  Alopecia, pruritus, scaling, lichenification esp along ventral midline
• tx: ivermectin, tx inflammation in eye PRN

• bovine herpesvirus 1 can cause conjunctival, respiratory, abortion, IPV, encephalitis, viremia.  They are SICK usu
• ocular presentation: uni or bilateral, acute serious conjunctivitis with epiphora, purulent d/c 1-3d later, mild to severe chemosis.  Raised white to reddish plaques on conjunctiva, coalesce. Possible peripheral corneal edema (IBK is central), non-ulcerative keratitis, secondary anterior uveitis

• tx: supportive, topical BSA if severe conjunctival dz
• prevention: vaccination, but will make IBK worse if already present
• prognosis: lesions resolve in 2-3wk, but can cause latency (STRESS)

Infectious bovine keratoconjunctivitis, aka Pinkeye

moraxella bovis (gram negative rod with 3 forms), mycoplasma bovoculi and more produce toxins, hemolysins, dermonecrolysins.  + inflammation = rapid tissue destruction (keratomalacia)

• any age bovine (usu 6-24mo), most don't get re-infected
• predisposing: UV!!  esp after snow, floods, decreased ocular pigment, irritants. NONE needed in virulent strains.  Worse around IBR outbreak times or vaccination.
• spread: face fly
• season: late spring/summer in young animals, winter in all animals

• NOT systemically ill
• sore, red eye (conjunctivitis) with epiphora, blepharospasm
• several animals at once
• unilateral or bilateral
• keratitis within 24-72h
• FOCAL CENTRAL EDEMA that ulcerates (IBR is peripheral)
• ulcers can be small or large and deep, abscesses, can persist for weeks.  Desmetoceles common, some will perforate (bovines are tough, give them time to heal). Can get reflex uveitis

vessels take 4-5days to be visible, then grow 1mm/day

• begin ASAP
• remove inciting causes, isolate affected (careful with Rx, some are illegal in food-producing)
• SID (b/c farmers won't do more): subconjunctival abx injection, topical abx, topical atropine, systemic oxytetracycline (approved, others used).  Tx ALL HERD.  
• Tx may not work, return to comfort important

• IBR: no corneal involvement acutely, corneal ulceration rare, peripheral edema, conjunctival plaques, systemically ill
• IBK: central edema, no conjunctival plaques, feel systemically fine
• Vax for IBR may cause IBK or make it worse

• chlamydophila/mycoplasma complex (NOT THE SAME as in cattle)
• no signalment, can be re-infected.  
• Uni or bilateral, intense conjunctivitis for 1-3d.  Epiphora, chemosis, hyperemic conjunctiva +/- hemorrhages, painful. Serous d/c turns mucopurulent after 3-4d, corneal edema, neovascularization, uveitis, polyarthritis, fever with chlamydophila.  Usu no ulceration
• Hallmark: follicular lymphoid hyperplasia and conjunctival folds hallmark of chlamydophilosis
• dx: exfoliative cytology of palpebral conjunctiva (intracytoplasmic inclusions in epithelial, culture (special for chlamydophila)

in utero BVD infection 76-150d = CNS anomalies (microencephaly, cerebellar hypoplasia, hydrocephalus, hydrancephaly) or eyes (microphthalmos, cataracts, retinal dysplasia, pigment changes, hemorrhage)

• common in ruminants if vertrum californicum ingested on gestational day 14-15
• This is happening in humans!!!  False hellebore ingested for morning sickness instead of true hellebore!

• 80% in some herds
• increased incidence after new male introduced
• tx: correct!  Rarely requires skin incision

uveitis is common in horses, caused by both lepto and borrelia!  Lepto MUCH more significant and causes RECURRENT (lepto, serovar pomona).  Vaccine now available

• deficiency can cause blindness in feedlot or growing cattle secondary to stenosis of optic canals
• clinical dz in young (blind, occurs a few months after serum vitamin levels fall

• wide spectrum of ocular defects seen in piglets of deficiency sows 
• anophthalmia, microphthalmia, cataract, retinal dysplasia, colobomas etc

• Tapetum: wavelengths transformed to best wavelength for species, then bounce to re-present to rods and cones
• rods: dim light vision, 1000s:1 so diffuse vision (scotopic, max sensitivity in darkness)
• cones: color and bright light, 1:1 in brain so detailed (photopic, max acuity in light)

• 3-neuron component.  
• Rods and cones outside, middle is translucent to allow light to pass through
• 1st-order electric current generated (pigment epithelium and photoreceptors layer), then 2nd (bipolar cells, layers 3-7) transmit/interneuron, 3rd (layers 8-10) ganglion cells next to vitreous collect and transmit through optic nerve to lateral geniculate nucleus.  
• LGN/optic radiation/visual cortex

• Choriocapillaris nourishes retinal pigment epithelium/outer layer
• retinal vessels nourish inner layer, on inner third.  
• Vary considerably
• Holangiotic (whole lot of vessels): primate, carnivore, ruminant, rat, mouse
• merangiotic (butterfly around disc): rabbit
• paurangiotic (tiny vessels, don't extend far. Some just a tuft): horse, guinea pig
• anangiotic (no visible vessels): bird, beaver, chinchilla, bat, reptile, amphibian

• Choroid underlies retinal pigment epithelium
• tapetum is inner layer of choroid.  Retinal pigment epithelium is not pigmented over tapetum

• Background: quality of tapetal reflections and non-tapetal area (brown or black)
• vessels: pattern and extent
• optic nerve head: size, shape, color and vascularity

Invagination of surface ectoderm causing optic cup.  Inside makes lens.  Retina: inner (9 layers of neural) and outer layer (pigmented retina) of optic cup. Potential space in between is area of detachment - just interdigitate with villi on retinal pigment epithelial cells. Electrostatic attachment.

• Detachment - separation in intraretinal space
• dysplasia - Panleuk, FeLV?, BVD
• dystrophy
• degeneration (primary = genetic, secondary can be metabolic, nutrition, sequelae)
• Metabolic (SARD and hyperthyroid)
• nutritional (taurine in cats, vitamin E in horse and dog, vitamin A)
• inflammation/infection
• trauma/toxicity

• Coloboma: embryological defect (paper punch hole) in tissue closure, typical at 6 o'clock (Last place it fuses, fetal fissure) and atypical anywhere else.
• dysplasia: abnormal formation. Classified by how much involved. photoreceptors only (genetic rod or rod-cone dysfunction) vs panretinal thickness dysplasia (multiple layers: folds (tiny), geographic (bigger), detachment/non-attachment (whole))

• Pushed off: exudative
• Pulled off: traction
• Perforated: torn
• There is also dysplasia, never attached at all - most common

Usually chorioretinitis too!

• Causes: inherited in dog, dif reasons in dif species?
• optic signs: vessel attenuation, altered tapetal reflectivity (tin foil), optic disc pallor, nontapetal fundus depigmentation, secondary cataract
• signs/progression: night blindness, mydriasis, day blindness, secondary cataract (late stages)

• sudden acquired retinal degeneration (SARD)
• optic neuropathy

• Sudden blindness, PUPD, polyphagia, weight gain, mydriasis, normal fundus initially
• ERG - absent!
• don't get better, just adjust

• "Sudden" blindness +/- disc swelling, mydriasis, normal fundus otherwise.
• Causes: GME, infections (mycoses or distemper), neoplasia (LSA)