VMED 7502: Ophthalmic Exam PDF

VMED 7502: Ophthalmic exam 1. Describe how to perform an ophthalmic examination including adnexa, globe, orbit, and reflexes; and interpret the examination findings when described in a clinical case scenario. a. Globe size i. Large-buphthalmos...

VMED 7502: Ophthalmic exam 1. Describe how to perform an ophthalmic examination including adnexa, globe, orbit, and reflexes; and interpret the examination findings when described in a clinical case scenario. a. Globe size i. Large-buphthalmos ii. Small- microphtalmos or phthsis bulbi b. Globe position i. Exophthalmos vs enophthalmos ii. Retropulsion 1. Contraindications- fragile globe, high IOP c. Menace response i. Assess vision and blink ii. Afferent: vision- retina, optic n. , optic tracts, visual cortex iii. Efferent: blink- facial nerve; motor to eyelids iv. Present around 10-12 wks of age in puppies and kittens d. Palpebral reflex i. Assess eyelid sensation and blink ii. Afferent: eyelid sensation- trigeminal nerve iii. Efferent: Blink- facial nerve; motor to eyelids iv. Inner corner- ophthalmic branch of CN 5 v. Outer corner- maxillary branch of CN 5 e. Pupillary Light Reflex i. Direct PLR & indirect or consensual PLR ii. Afferent: retina & CN 2 iii. Efferent: CN 3 & iris sphincter m. iv. Does not assess vision 2. Select ophthalmic diagnostic tests appropriate for a given history, signalment and clinical signs, and accurately interpret the results. 3. Demonstrate correct technique, and identify incorrect technique, in basic ophthalmic exam procedures and performing basic diagnostic tests. a. Indirect ophthalmoscopy i. Advantages: 1. Larger field of view 2. Better view through opacities in clear media 3. Viewer has depth perception 4. Farther from patient’s face ii. Disadvantages 1. Image is upside down and reversed 2. Learned technique b. Direct ophthalmoscopy i. Advantages: 1. Easy to perform 2. Image is upright 3. Magnified image ii. Disadvantages 1. Very small field of view 2. Any opacities interfere with view  3. Close to patient’s face 4. Recall contraindications for performing specific ophthalmic diagnostics, and for use of proparacaine and tropicamide. a. Tropicamide- dilation b. Proparacaine- topical anesthesia 5. Schirmer Tear Test- Dogs >15mm/min a. Basal tears + reflex tears i. Afferent= corneal sensation ii. Efferent= parasympathetic fibers of CN 7 to lacrimal gland 6. Tonometry- requires topical anesthesia (proparacaine) a. Dogs- 10-25mmHg b. Cats- 10-30mmHg c. Horses- 15-30mmHg d. Similar values between OD & OS i. Less than or equal to 5mmHg difference 7. Hallmark of inflammation in the eye= uveitis Neuro-ophthalmology Learning Outcomes Following this lecture, students will be able to: 1. Assess vision using various techniques and differentiate between vision loss and abnormal mentation a. b. Dazzle- blink in response to very bright light 2. Interpret pupillary light reflex (PLR) abnormalities and localize lesions based on direct and consensual PLR a. Afferent: sensory i. Going toward CNS b. Efferent: motor i. Going away from CNS c. Retina -> optic nerve -> crossover at optic chiasm -> optic tract -> oculomotor nerve (III) -> ciliary ganglion -> parasympathetic supply to the iris 3. Diagnose anisocoria and determine which of the pupils is abnormal a. Anisocoria- unequal pupil size b. Pupillary light reflex c. Increasing or decreasing room light i. Lack of parasympathetic innervation: increasing room lighting will cause normal pupil to constrict, which will create a more obvious anisocoria since the abnormal pupil cannot constrict ii. Lack of sympathetic innervation: decreasing room lighting will cause the normal pupil to dilate, which will create a more obvious anisocoria since the abnormal pupil cannot dilate 4. Formulate a differential list of neurologic and ophthalmic causes of anisocoria a. Rule outs:  i. Synechia ii. Congenital iris anomalies iii. Iris atrophy iv. Uveitis v. Glaucoma VMED 7502: Ocular Pharmacology 1. Determine appropriate route of drug administration is appropriate based on the part of the eye or adnexa affected a. Drugs applied topically will not penetrate beyond the lens i. Will not reach vitreous, retina, choroid, optic nerve ii. Depending on the drug, some do not penetrate through the cornea b. Ointments i. Provide longer lubrication ii. Easier to administer in large animals iii. Greasy film around eye iv. Contraindicated in deep corneal ulcers, perforation, or laceration c. Solutions i. Easier to administer in small animals ii. Travels through nasolacrimal duct more easily than ointment d. Topical meds i. Always wait at least 5 min btwn eye drops ii. One drop per dose iii. Order of meds: 1. Soln in aqueous base 2. Soln in oil base 3. Ointments e. SPL i. Large animals ii. Painful eye iii. Frequent tx f. Subconjunctival injections i. Bulbar conjunctiva ii. When topical therapy is not strong enough  1. Keratitis 2. Scleritis 3. Anterior uveitis iii. Single tx (cattle) g. Implants (cyclosporine) i. Episcleral (subconjunctival) 1. Immune-mediated keratitis (horses) 2. Dry eye disease (dogs) 3. Pannus (dogs) ii. Suprachoroidal 1. Equine recurrent uveitis 2. Classify common ophthalmic drugs based on the disease each is intended to treat a. Topical antibiotics i. Gentamicin ii. Neomycin/polymixin B/ bacitracin iii. Neomycin/polymixin B/ gramicidin iv. Tobramycin v. Erythromycin vi. Cefazolin 50 mg/ml vii. Oxytetracycline/polymixin B viii. Fluoroquinolones (ofloxacin, ciprofloxacin, moxifloxacin) 1. Never use as first line antibiotic choice. Reserved for infected corneal ulcers/abscess 2. Can penetrate through intact corneal epithelium ix. Chloramphenicol b. Systemic antibiotics i. Clavamox 1. Broad spectrum 2. Ineffective against pseudomonas ii. Cefpodoxime 1. Gram + and some gram neg coverage iii. Enrofloxacin 1. Predominantly gram neg 2. DO NOT USE IN CATS- retinal degeneration iv. Doxycycline 1. Effective against rickettsial organisms 2. Good for lepto c. Topical antifungals i. Voriconazole 1% ii. Miconazole 1% iii. Natamycin 5% iv. Silver Sulfadiazine v. Amphotericin B 1. Admin subconjunctivally d. Systemic antifungals i. Fluconazole 1. Equine corneal infection 2. Disseminated fungal disease in dogs and cats  ii. Itraconazole 1. Do not use compounded formulation e. Topical Antivirals i. Cidofovir 0.5% ii. Idoxuridine 0.1% iii. Trifluridine 1% f. Systemic antivirals i. Famciclovir g. Steroids and Nonsteroidals (NSAIDs) i. NSAID: anterior and posterior uveitis ii. Steroid: anterior and posterior uveitis h. Topical steroids i. Prednisolone acetate 1% 1. Best intraocular penetration ii. Dexamethasone 0.1% 1. With neomycin/polymixin B iii. Hydrocortisone 1%/ neomycin/ poly B 1. Does not penetrate cornea i. Topical NSAIDs i. Diclofenac 0.1% ii. Flurbiprofen 0.03% iii. Ketorolac 0.5% Glaucoma Drugs j. Prostaglandin analogs i. Increase outflow through less common uveoscleral pathway ii. Iatanoprost iii. Travoprost iv. Bimatoprost k. Carbonic anhydrase inhibitors i. Dorzolamide ii. Brinzolamide l. Beta adrenergic blockers i. Timolol 0.25% ii. Timolol 0.5% m. Proparacaine, tetracaine i. NEVER prescribe this medication 1. Toxic to corneal epithelial cells with repetitive use 3. Recognize contraindications for specific ophthalmic drugs a. Never use a systemic steroid and NSAID together -> serious risk of GI ulceration/perforation b. Can use a topical steroid and topical NSAID together c. Can use a topical steroid and systemic NSAID/ topical NSAID and systemic steroid d. Can use a topical steroid and systemic steroid/ topical NSAID and systemic NSAID e. Systemic NSAIDS do have analgesic effects; topical NSAIDs do not have analgesic effects on eye f. Topical steroids contraindications i. Corneal ulcer ii. Corneal stromal abscess  iii. Active infection (cornea, conjunctiva) 1. FHV 2. EHV 3. Equine keratomycosis g. Topical NSAID contraindications i. Hyphema ii. Glaucoma iii. Corneal ulcer h. Prostaglandin contraindications i. Glaucoma secondary to anterior uveitis ii. Glaucoma secondary to anterior lens luxation Orbit LO 1. Identify clinical signs consistent with orbital disease a. Enophthalmos i. Globe sunken into orbit ii. Elevated nictitating membrane iii. Decreased palpebral fissure size iv. Causes 1. Pain 2. Horner's syndrome 3. Decreased masticatory muscle mass b. Exophthalmos i. Most common sign of orbital disease ii. Anterior displacement of the globe iii. Caused by space occupying effect in the retrobulbar space iv. Clinical signs 1. Globe protruding anteriorly 2. Increased palpebral fissure size 3. Elevated nictitating membrane 2. Differentiate characteristic clinical signs of inflammatory versus neoplastic etiologies of orbital disease a. Inflammatory i. Signalment: young  ii. Acute onset iii. Painful retropulsion or when opening mouth iv. Periocular inflammation v. Unilateral 1. Retrobulbar abscess 2. Orbital cellulitis 3. Mucocele 4. Hematoma vi. Bilateral 1. Myositis b. Neoplastic i. Signalment: old ii. Gradual onset iii. Non-painful retropulsion or opening mouth iv. Absence of periocular inflammation v. Carcinoma vi. Sarcoma vii. Lymphoma viii. Meningioma ix. Canine lobular orbital adenoma 3. Develop an appropriate diagnostic and treatment plan for a patient presenting for orbital disease a. Diagnostics i. Ocular ultrasound ii. Computed tomography or magnetic resonance iii. Dental or skull radiographs b. Treatment i. Myositis 1. Immunosuppressive therapy ii. Retrobulbar abscess/cellulitis 1. Systemic antibiotics 2. Systemic NSAID 3. +/- opioids for additional analgesia 4. +/- opening for drainage iii. Neoplasia 1. Extension from nasal sinuses -> treat primary neoplasia 2. Metastatic -> treat primary neoplasia 3. Primary -> exenteration iv. Mucocele 1. Drainage 2. Anti-inflammatory therapy 3. Excision of cyst and associated gland 4. Evaluate a globe proptosis and determine whether enucleation or temporary tarsorrhaphy is the appropriate recommendation a. Enucleate i. Optic nerve is severed ii. Globe is ruptured iii. Cornea severely desiccated/ulcerated  iv. More than 2 extraocular m. torn b. Temporary tarsorrhaphy i. If there is a chance to save the EYE (does not = vision) Adnexa 1. Diagnose conformational abnormalities of the eyelid and recognize clinical scenarios that require permanent or temporary correction a. Trichiasis i. Hair growing from normal location in abnormal position ii. Entropion, nasal fold, medial canthal b. Distichiasis i. Hair growing from meibomian gland -> emerges from meibomian gland opening ii. Clinical Signs: corneal irritation, epiphora iii. Tx: cryoepilation c. Ectopic cilia i. Hair growing from meibomian gland -> emerges from palpebral conjunctiva ii. Clinical signs: corneal ulceration, pain iii. Tx: excision of the hair and associated follicle followed by cryotherapy d. Ectropion i. Eyelid rolling outward; normal conformation in some breeds; surgical correction if causing disease e. Entropion i. Eyelid rolling inward; causes epiphora, blepharospasm, corneal ulceration ii. Temporary correction: temporary tacking sutures 1. Indicated for: puppies or spastic entropion iii. Surgical correction: must be skeletal mature 1. Do not over-correct! 2. Hotz-Celsus procedure 2. Formulate a differential list of common eyelid tumors and adjust the treatment plan based on species, size, and location of the mass a. Canine eyelid neoplasia i. Meibomian gland adenoma 1. Melanocytoma, papilloma, histiocytoma, mast cell tumor, scc b. Canine inflammatory diseases i. Chalazion 1. Blockage of meibomian gland ii. Pyogranulomatous blepharitis 1. Sterile or associated with staph infections 3. Identify anatomic components of the eyelid and nictitating membrane and predict their contribution to ocular health a. Blepharitis i. Inflammation of the eyelids ii. Allergic, immune mediated, demodex b. Nictitating membrane i. Covered with conjunctiva ii. T-shaped cartilage iii. Important to ocular surface health iv. Protection of globe v. Helps to move debris off surface of cornea vi. Lacrimal gland produces up to half of the aqueous component of tear film 4. Recognize clinical signs consistent with keratoconjunctivitis sicca (KCS), perform appropriate diagnostics, and initiate a therapeutic plan a. Dry eye disease  b. Decreased production of the aqueous component of the tear film c. Clinical signs i. Conjunctivitis ii. Mucopurulent discharge iii. Dull, lackluster appearance of cornea iv. Keratitis: vascularization, pigmentation, fibrosis, ulceration 1. Ulceration: acute 2. Pigmentation/fibrosis: chronic v. Blepharospasm d. Disease of Dogs i. Most common etiology: immune-mediated lacrimal gland adenitis ii. Diagnosed with Schirmer tear test and consistent clinical signs iii. Always measure both eyes iv. Always perform fluorescein stain with KCS- high risk of ulcer e. Tx i. Cyclosporine or Tacrolimus ii. Immunosuppressive class of drugs iii. Stimulates tear production in immune-mediated KCS by inhibiting T helper lymphocytes in the gland iv. Improves comfort and decreases in discharge v. Can be used with corneal ulcers vi. Can break-up corneal pigment over long-term use vii. Can never be stopped f. Tx: neurogenic i. Pilocarpine (dilute) ii. Not always effective iii. Can also be administered orally on food g. Tx- regardless of etiology i. Topical antibiotic for bacterial overgrowth ii. Topical lubricant 5. Locate the components of the nasolacrimal drainage system and describe expected clinical signs and diagnostics to diagnose nasolacrimal disease a. Lacrimal puncta i. Superior and inferior b. Canaliculi i. Superior and inferior c. Lacrimal sac d. Nasolacrimal duct e. Nasal puncta f. Assess patency of drainage i. Fluorescein dye -> passive drainage ii. Flushing NLD through puncta iii. Dacryocystohinography g. Clinical Signs i. Epiphora (most common) 1. Result of either a. Increased tear production b. Decreased tear drainage via the nasolacrimal system ii. Mucopurulent discharge iii. Abnormal tear drainage 1. Imperforate puncta 2. Inflammation of nasolacrimal duct 3. Stricture or fibrosis within the duct Cornea 1. Relate basic corneal anatomy and physiology to corneal disease/pathology. 2. Systematically rule out etiologies for corneal disease based on signalment, history and clinical examination findings in a clinical case scenario. 3. Select ophthalmic diagnostic tests appropriate for a given history, signalment and clinical signs, be able to justify the selections, and accurately interpret the results. 4. Recognize and interpret clinical signs of corneal disease including presence/absence of pain, chronicity, severity, and clinical prognosis for vision and for the eye. 5. Formulate an appropriate treatment plan for a corneal condition/disease including, when appropriate, levels of treatment from ideal to palliative including referral procedures and be able to justify your recommendation(s). 6. Recognize, and formulate a treatment plan for, the clinical signs of intraocular disease secondary to corneal disease. Topic: Lens 1) Relate basic lens anatomy and physiology to nuclear sclerosis, cataract formation, and lens luxation. a) Nuclear sclerosis i) Normal aging change ii) Compressed lens fibers in center of lens iii) Does not interfere with vision b) Cataract formation i) Loss of clarity ii) Result of alteration in water, electrolyte, protein content in lens iii) Dogs >>>horses>cats iv) Genetics- Most common (1) Young to middle aged (2) Commonly bilateral w/ staggered onset v) Diabetes Mellitus- 2nd most common (1) Acute onset (2) Very common in diabetic dogs (3) Hyperglycemia -> increased glucose in aqueous humor (4) Increased glucose diffuses into lens-> overwhelms hexokinase (5) Glucose shunted to aldose reductase pathway -> converts to sorbitol 2) Diagnose a cataract by performing a complete ophthalmic exam, identify etiology and stage of cataract, facilitate referral, and formulate a treatment plan. a) Cataract diagnosis i) PLR should be normal regardless of stage ii) Mydriasis iii) Retroillumination and illumination b) Advanced cataracts -> alteration of lens composition -> leakage of lens proteins through capsule -> uvea exposed to lens protein -> inflammation i) MUST begin topical anti-inflammatories c) Treatment i) Surgical- photoemulsification w/ intraocular lens implants (1) No medical treatment ii) Refer early iii) Start anti-inflammatory eye drop 3) Explain pathogenesis and sequelae of phacolytic and phacoclastic uveitis. a) Phacolytic uveitis- most common b) Phacoclastic- lens capsule rupture c) Sequelae i) Secondary glaucoma  ii) Retinal detachment iii) Posterior synechia- adhesions 4) Formulate an appropriate treatment plan for a patient with a lens luxation based on signalment, chronicity, underlying etiology, and prognosis for vision. a) Anterior lens luxation = ER situation i) Anterior lens luxation- acute glaucoma (pupillary block) ii) Intracapsular extraction iii) Transcorneal reduction iv) Complications: secondary glaucoma; retinal detachment b) Posterior lens luxation: managed w/ miotics 5) Educate clients regarding referral options for cataract surgery, lens luxation, and traumatic lens capsule rupture. VMED 7502: Uvea & manifestations of systemic disease 1. Recognize common non-inflammatory uveal conditions (iris atrophy, iris cyst, persistent pupillary membranes) based on history, signalment and clinical signs. a. Iris atrophy i. Normal aging change in geriatric dogs and cats ii. Not pathologic iii. Appears as an irregular thinning of the iris at the pupil; or can be as advanced as holes in the iris iv. Causes an EFFERENT PLR deficit v. b. Uveal cysts i. From the posterior pigmented epithelium of the iris and ciliary body ii. Non pathologic 1. EXCEPT in Goldens, american bulldogs, great dane iii. Locations within the anterior chamber 1. Attached at the pupil margin 2. Floating in the ventral anterior chamber 3. Ruptured cysts appear on the corneal epithelium iv. Differential diagnosis from melanoma  1. Cysts are smooth and round 2. Cysts transilluminate Transillumination v. c. Persistent Pupillary membranes (PPM) i. Congenital ii. Remnants of blood vessels spanning the pupil in embryonic development -> as the eye develops there is not complete atrophy of the membrane tissue iii. Iris to iris (most common): not clinically significant iv. Iris to lens or iris to cornea (uncommon): can be clinically significant if it results in a large lens or corneal opacity at the point of attachment v. d. Uveal neoplasia i. Canine (melanocytoma) 1. Benign but locally invasive 2. If large usually enucleate globe once secondary glaucoma develops and the eye is blind, painful ii. Feline (melanomas) 1. Higher metastatic potential iii. Lymphoma-> causes severe uveitis typically 1. Diffuse iris infiltration 2. Hemorrhagic  3. 2. Relate normal anterior and posterior uveal anatomy and physiology to the pathogenesis of uveitis and hemorrhagic conditions. a. Anterior uveitis- affecting iris & ciliary body i. Hypotony: low IOP ii. Miotic pupil- Constricted iii. Aqueous flare- cells and proteins in aqueous humor iv. Iris color change & swelling; edema; WBC infiltrate; engorged vessels b. Posterior uveitis- affecting choroid (chorioretinitis) i. Choroidal exudates and retinal detachment 1. Cells, fluid, proteins enter subretinal space ii. Retinal and choroidal hemorrhages 1. Inflammation or direct vessel damage 2. Vision loss= retinal detachment c. Inflammation of entire uveal tract- panuveitis 3. Recognize the clinical signs of anterior uveitis and chorioretinitis in a clinical scenario including written description and picture. Retinal Detachment: animal would be a. blind! Posterior uveitis- abnormal hazy, gray b. 4. Developareas a logical list of etiologies for cases of uveitis, and cases of intraocular hemorrhage without uveitis, using signalment, history, and ophthalmic and physical examination findings; and recommend and justify appropriate diagnostic tests.  a. Corneal injury= reflex uveitis b. Lens-induced uveitis i. “Phacoclastic is drastic” c. Trauma- blunt force or penetrating injury d. Immune-mediated: ERU, steroid responsive retinal detachment e. Idiopathic- MOST COMMON f. Other: Golden retriever pigmentary uveitis & uveodermatologic syndrome i. Golden retriever pigmentary uveitis 1. Pigmented deposits on lens capsule, bilateral iris and ciliary body cysts, posterior synechia, flare, fibrin, secondary glaucoma ii. Uveodermatologic syndrome 1. Immune mediated; melanocytes 2. Akitas are predisposed 3. Severe bilateral uveitis with retinal detachment 4. Derm signs: depigmentation, ulceration mucocutaneous junctions 5. Diagnosis: negative for infectious disease; histopath g. Anything systemically that can cause vasculitis has potential to manifest with uveitis inside of the eye i. Vasculitis -> breakdown of blood-aqueous and/or blood-retinal barrier -> clinical signs of uveitis ii. Infectious 1. Bacterial 2. Fungal 3. Viral- think about cats 4. Protozoal 5. Algal 6. Parasitic iii. Neoplasia iv. Immune-mediated v. Idiopathic- ultimate cause of uveitis 5. Based on the treatment principles for uveitis, formulate a treatment plan for a patient, justify each treatment, and identify any contraindications for medication(s) in the patient. a. General principles i. Suppress inflammation 1. Topical corticosteroids 2-6x per day  a. Prednisolone acetate, NeoPolyDex b. Contraindications: corneal ulcers/abscesses, infectious corneal diseases 2. Topical NSAIDs a. Diclofenac, flurbiprofen, keterolac b. Not sufficient for most cases of uveitis alone c. Contraindications: corneal ulcers, glaucoma ii. Prevent synechiae 1. Topical atropine a. Dilates pupil b. Paralyzes ciliary muscle spasm thereby decreasing pain c. Contraindications: glaucoma, lens instability d. Side effects: hypersalivation, colic 2. Systemic and topical NSAIDs (anti-prostaglandin effect) iii. Eliminate underlying cause 1. Thorough ophthalmic exam 2. Physical exam 3. Diagnostic test 4. Treat underlying cause AND uveitis iv. Systemic route of medication MUST be used for posterior uveitis 1. Systemic anti-inflammatory- immune-mediated chorioretinitis/retinal detachment a. Prednisone, prednisolone b. Do better than NSAIDs in cases of uveitis 2. NSAIDs a. Carprofen, meloxicam, flunixin meglumine b. Infectious causes of uveitis c. Provides analgesia 3. NEVER use systemic steroid and NSAID together  v. History -> Ophthalmic diagnostics -> PE & Ophthalmic exam -> decide primary ocular or systemic dz vi. Primary ocular? 1. Treat the eye vii. Systemic dz 1. Ophthalmic signs 2. Systemic diagnostics: CBC, chem, UA 3. Ocular diagnostics: FNA of iris, vitreous aspirate 6. Anticipate the complication of secondary glaucoma in a patient with anterior uveitis, and recognize the clinical signs associated with the risk of secondary glaucoma. 7. Recognize the ophthalmic clinical signs associated with common metabolic and blood/vascular systemic diseases. a. Lipemic flare i. Hyperlipidemia 1. Primary hyperlipidemia – mini schnauzers 2. Secondary- endocrine disorders, pancreatitis, cholestasis, protein-losing nephropathy, obesity, and high fat diets ii. Must also have a reason for uveitis iii. Sudden onset, white cloudy eye +/- vision loss iv. Initiate topical treatment v. Address underlying causes vi. Usually resolves very quickly b. Intraocular hemorrhage i. Retinal detachment 1. Giant retinal tears- shih tzus 2. Systemic hypertension ii. Clotting disorder  1. Thrombocytopenia 2. Rodenticide tox 3. Liver failure 4. Inherited disorders iii. Uveitis iv. Intraocular neoplasia v. Trauma VMED 7502: Fundus 1. Recognize normal variations in the ocular fundus of common domestic species. a. Tapetum i. Dorsally located & roughly triangular in shape ii. May be absent iii. Color- blue/purple tapetum in young puppies b. Pigment i. Normally found in retinal pigmented epithelium and choroid ii. Degree of pigmentation can vary iii. Dilute animals & blue eyes = subalbinotic 1. 2. Relate retinal and choroidal anatomy and physiology to the appearance of normal variations of the fundus on ophthalmic examination, and to the pathogenesis of chorioretinitis, hemorrhage and retinal detachment.  a. b. Chorioretiniti c. 3. Recommend appropriate referral for electroretinogram and ocular ultrasound, explain the purpose of each, and justify for that patient. a. Electroretinogram i. Tests function of retina ii. Tests for retinal degeneration 1. Fundus is not visible 2. Possible diagnosis of Sudden Acquired Retinal Degeneration b. Ocular Ultrasound i. Images the position of the retina if it is not visible on fundic exam ii. Diagnostic used for retinal detachment 4. Recognize the clinical signs of retinal degeneration and conclude the most likely etiology based on signalment, history and clinical signs. DETACHMENT a. Rhegmatogenous = tear i. Retinal tear ii. Can tear from natural attachments or get a hole iii. Etiologies 1. Vitreal degeneration (shih tzu, italian greyhound, whippet)  2. Retinal dysplasia- congenital 3. Collie eye anomaly- congenital 4. Lenticular disease 5. Post-inflammatory iv. Treatment 1. Only treatment is referral for retinal reattachment surgery b. Non-rhegmatogenous i. No retinal tear ii. Aka “bullous” retinal detachment (parachute game) 1. Subretinal transudate or exudate 2. Completely attached at normal attachment sites 3. Tapetal hypo-reflectivity iii. Etiologies 1. Systemic hypertension a. 2. Chorioretinitis (infectious, neoplastic, immune-mediated) 3. Steroid-responsive iv. Treatment 1. Treat underlying cause 2. Retinal can reattach- may regain vision if not too far gone DEGENERATION- degeneration of one or more layers of the retina 1) Thinning of retinal tissue 2) Tapetal hyperreflectivity 3) Attenuation of retinal blood vessls 4) +/- optic nerve head atrophy 5) Causes a) Inherited- progressive retinal atrophy (PRA) b) Sudden Acquired Retinal Degeneration Syndrome (SARDS) c) Prolonged retinal detachment d) Chronic glaucoma e) Any form of chorioretinitis f) Drug-associated  g) Nutritional h) Senile 6) progressive retinal atrophy (PRA)- inherited a) Loss photoreceptors i) Rods first- loss of night vision first (nyctalopia) ii) Cones later b) Retinal degeneration noted on fundic exam c) No systemic signs d) Diagnosis: history, fundic exam, +/- ERG e) PLR- slow, incomplete i) End: could be absent f) 7) SARDS a) Loss of all photoreceptor function b) At initial presentation, fundic exam is normal c) Concurrent cushingoid signs possible (PU/PD) d) Diagnosis: ERG e) Differential: central blindness (brain) f) 8) NO BAYTRIL IN CATS- associated with retinal degeneration 9) Nutritional- Taurine deficiency in cats a)  10) Chorioretinal scars a) Areas of previous inflammation i) Focal retinal thinning ii) Pigment clumping and/or tapetal changes common iii) No current active disease iv) 11) Optic Disk (Optic nerve head) a) Feline i) Non-myelinated ii) Vessels do not cross the disc b) Canine i) Amount of myelin varies creating a round to triangular shape, gray to white color ii) Vessels cross the disc structure c) Horse i) Large, horizontal oval d) Ruminant i) Dark, tannish color causing it to blend into background, to cream colored depending on species ii) Extremely large overlying vessels 5. Recognize optic neuritis by clinical signs. a. Blind b. Fixed, dilated pupils c. Swollen, enlarged d. Hyperemia optic neuritis e. (chronic) GLAUCOMA 1. Understand the underlying anatomy and physiology of aqueous humor production and outflow and how this relates to glaucoma. a. Aqueous humor is produced by ciliary body i. AH provides nourishment for avascular intraocular structures b. AH moves anteriorly through the pupil to exit through the iridocorneal angle i. Conventional pathway 1. ICA -> trabecular meshwork -> scleral veins ii. Uveoscleral pathway 1. Ciliary body musculature -> suprachoroidal space -> scleral veins 2. Recognize common history and signalment for dogs with primary glaucoma. a. Abnormal iridocorneal angle i. Primary glaucoma ii. Goniodysgenesis (pectinate ligament dysplasia) 1. Puppy born with abnormally formed iridocorneal angle iii. Closed angle glaucoma more common than open angle glaucoma in dogs b. Intraocular pressure i. AH production and outflow should be in perfect balance to maintain normal IOP 1. Normal IOP = 10-20 mmHg 2. High BP has NO correlation to IOP ii. Glaucoma develops due to impaired outflow iii. Increased IOP damages: 1. Optic nerve 2. Retina 3. Cornea 4. Iris c. Signalment i. Middle age (6-8 yo) ii. Bilateral but not at same time iii. Primary glaucoma- breed related 1. American cocker spaniel, bassets, chow chow, shar-pei, boston terrier, fox terrier, siberian husky d. History i. Blepharospasm, nictitating membrane protrusion, red eye, cloudy eye, mydriasis, decreased vision, lethargy 3. Recognize and understand the pathogenesis behind the common clinical signs of glaucoma.  a. Clinical Signs i. Blindness ii. Acute blepharospasm iii. Episcleral injection iv. Corneal edema v. Mydriasis vi. Chronic buphthalmos vii. Lens subluxation or luxation viii. Optic nerve and retinal degeneration 4. Review the various methods of tonometry and proper technique for each method a. Indirectly measures IOP via: i. Rebound- speed at which probe returns to resting position ii. Applanation- pressure required to flatten cornea b. Proper technique i. No pressure on globe ii. Keep eyelids open by resting fingers on orbital rim iii. Stabilize hand iv. Measure normal cornea v. Corneal contact should be in the center of the cornea and perpendicular to the cornea 5. Be able to recognize acute vs. chronic clinical signs of glaucoma. Acute Chronic Blindness (may be reversible) Blindness (non-reversible) Episcleral injection Episcleral injection Normal globe size Buphthalmos Blepharospasm Blepharospasm uncommon Corneal edema Corneal edema Mydriasis Mydriasis Fundic exam is normal Fundic exam abnormal o ONH cupping, atrophy o Retinal degeneration 6. Understand the mechanism of action and contraindications for common anti-glaucoma medications. a. Prostaglandin analogues (topical) i. Latanoprost (q 12-24 hrs) 1. Facilitates aqueous humor outflow via unconventional pathway 2. Potent miotic 3. First choice for acute primary glaucoma in dogs  a. Begins to lower IOP within in 40 minutes ii. Contraindications 1. Anterior lens luxation 2. Glaucoma secondary to uveitis b. Carbonic anhydrase inhibitors (TID) i. Dorzolamide; brinzolamide (topical) ii. Methazolamide (oral)- DO NOT USE IN CATS 1. Side effects: GI upset, metabolic acidosis, hypokalemia iii. Decrease aqueous humor production c. Beta adrenergic antagonists - “beta blockers” - topical i. Timolol (BID) ii. Decrease aqueous humor production iii. Caution: bradycardia, bronchoconstriction d. Hyperosmotic agents: acute glaucoma i. Mannitol (IV slowly) 1. Lowers IOP within 30-60 min 2. Lasts 6-10 hours ii. Glycerin (oral) 1. Lower IOP within 1 hour 2. Lasts 6-10 hrs iii. Contraindications: heart dz, renal dz, dehydration, diabetes (glycerin) iv. Only use if latanoprost is ineffective 7. Recognize the indications for referral glaucoma surgeries (cyclophotocoagulation or gonioimplant) and end stage glaucoma surgeries (enucleation, evisceration, chemical ablation). a. Decrease production of aqueous humor i. Diode laser cyclophotocoagulation: damages the ciliary body tissue to decrease aqueous humor production -> lower intraocular pressure ii. Side effects: associated with severe intraocular pressure b. Increase aqueous humor outflow i. Filtering implants (gonioimplants): provide new pathway for aqueous outflow ii. Fibrosis limits long term success Chronic glaucoma- end stage procedures c. Enucleation d. Evisceration- refer i. Removal of intraouclar contents and placement of intrascleral prosthesis ii. Should never be used in cases of intraocular neoplasia  iii. Complications: KCS, corneal ulcers e. Chemical ablation i. Injection of gentamicin (epithelio-toxic) into vitreal compartment ii. Approx 85% effective iii. NEVER in cats or cases of intraocular neoplasia iv. Globe typically becomes phthisical (shrunken) 8. Understand the treatment principles for primary glaucoma based on potential for vision and goal of comfort. a. Affected eye is permanently blind i. Goal is COMFORT ii. End stage procedure iii. Medications can be used until the IOP becomes refractory to maximal medical therapy b. Affected eye has potential for regaining vision i. True ophthalmic sx ii. Latanoprost immediately 1. Dorzolamide TID 2. Timolol BID iii. Combine medical and sx therapy if client is interested in referral c. Fellow “unaffected” eye- predisposed to glaucoma i. Postpone onset of glaucoma ii. Timolol or dorzolamide BID iii. Routine IOP recheck (q 2-3 mo) iv. Client education 9. Be able to differentiate between primary and secondary glaucoma and recognize the potential causes of secondary glaucoma. Secondary glaucoma a. Causes i. Anterior lens luxation -> blocks flow of AH through the pupil ii. Primary intraocular neoplasia -> space occupying mass, obliteration of drainage angle iii. Uveitis 1. Acute: blood, fibrin, cells clogging in the iridocorneal angle 2. Chronic: 360 degree posterior synechia-> pupillary block -> iris bombe 3. Chronic: pre-iridial fibrovascular membrane -> crosses over iridocorneal angle iv. Hyphema  b. Treatment i. Enucleation if permanently blind 1. Submit globe for histopath ii. Anterior lens luxation -> referral iii. Primary intraocular neoplasia -> enucleation iv. Uveitis -> topical steroid, systemic steroid or NSAID 1. Carbonic anhydrase inhibitors and timolol safe to use v. Hyphema -> same as uveitis 10. Be able to counsel client regarding prognosis for glaucoma. a. Primary i. No cure ii. Goal is to preserve vision and comfort for as long as possible iii. Blind dogs can still have excellent quality of life b. Secondary i. Prognosis for vision is guarded in most cases ii. Must address underlying cause Topic: Feline ophthalmology 1. Develop a differential list for feline conjunctivitis and/or keratitis and formulate a plan that includes appropriate diagnostic tests, therapeutic recommendations and follow-up recommendations Feline Herpesvirus 1 o Most common cause of feline conjunctivitis o First exposure: upper respiratory dz, severe conjunctivitis, corneal ulceration o Neonatal: Bilateral -> often have respiratory clinical signs o Acute/chronic: juvenile or adult -> may be unilateral or bilateral o Recurrent: Adult recurrence due to latency -> often unilateral o Antiviral: Famciclovir- wide margin of safety; NEVER use other oral antivirals in cats- some are toxic Chlamydophila o No keratitis or corneal ulceration o Chemosis, serous to mucopurulent ocular discharge, conjunctivitis, mild respiratory signs; often presents initially unilaterally o Diagnosis: Conjunctival cytology, PCR o Tx: topical erythromycin, systemic tetracyclines Mycoplasma o No keratitis or corneal ulceration o Chemosis, conjunctivitis, +/- mild respiratory signs o Diagnosis: Conjunctival cytology, PCR o Tx: topical erythromycin, systemic tetracyclines Calicivirus o Look for oral ulcerations o Diagnosis: PCR o Tx: antivirals ineffective, supportive tx  2. Identify ophthalmic clinical signs that may be manifestations of a systemic disease process Conjunctivitis Corneal ulcer Sneezing/nasal discharge Hyphema 3. List adverse effects of oral fluoroquinolones and topical polymyxin B in cats Enrofloxacin- associated retinal toxicity o Tapetal hyper-reflectivity o Thin retinal vessels o PLR slow/incomplete or absent o Most are irreversibly blind Polymyxin B o Anaphylactic event within 4 hours 4. Describe the pathogenesis of feline diffuse iris melanoma and how this disease differs from uveal melanoma in dogs Most common intraocular tumor in cats o Progressive disease o Typical unilateral o Recheck q 3 months o Tx: diode laser, iridal biopsy, enucleation Topic: Equine Ophtho 1. Recognize which nerve blocks are commonly performed during an equine ophthalmic exam and when each is indicated Auriculopalpebral block o Blocks motor to the upper eyelid o Does not impact sensory of the eyelid Supraorbital block o Blocks sensory innervation to the upper eyelid o Frontal nerve is blocked as it exits supraorbital foramen Lower eyelid- zygomatic, infratrochlear 2. Identify the most common locations and appearance of equine periocular squamous cell carcinoma, appropriate treatment and prognosis, as well as preventative strategies Depigmented face/eyelid margin predisposed UV light exposure  Avg age is 9-12 years Locations o Eyelid o nictitating membrane: red/pink nodule or proliferative mass, excision of entire nictitans is generally curative o bulbar conjunctiva +/- limbus and cornea Eyelid SCC carries worst prognosis o Cannot perform complete excision o Highest risk of local invasion o Highest risk of metastasis Treatment o Debulking/adjunctive therapy 1. Cryotherapy, immunotherapy, CO2 laser ablation, Intralesional chemo, piroxicam o Photodynamic therapy 3. Develop a diagnostic and treatment plan for ulcerative and non-ulcerative keratitis in the horse Non-ulcerative o Topical abx o Systemic NSAID o Atropine o Recheck 5-7d Ulcerative- infected- SPL o Topical abx- fluroquinolones (ofloxacin) o Topical antifungal o Anticollagenase- serum o Atropine o Systemic therapy (banamine) o Systemic abx o Systemic antifungal (fluconazole) 4. Discuss the proposed pathogenesis of Equine Recurrent Uveitis (ERU), diagnostics indicated for this disease, and strategies for treatment Immune-mediated Clinical classification o Classic recurrent o Insidious o Posterior uveitis  Suppress inflammation, prevent synechia (atropine), treat underlying cause if identified Topic: Exotics 1. Identify husbandry factors contributing to ocular disease in exotic species Humidity & temperature i. Retained spectacle 2. Assess the risk of systemic absorption of topically applied medications in common exotic pet species Systemic paralysis 3. Recall unique ocular anatomic structures in common exotic pet species Birds & Reptiles i. Scleral ossicles ii. Posterior scleral cartilage 1. Flat- psittacines & passerines 2. Globoid- large diurnal raptors 3. Tubular- owls Glands i. 3-4 glands present in orbit ii. Harderian gland may secrete porphyrins- rodents Orbital venous sinus i. Particularly large in rabbits Eyelids i. Snakes and most geckos have fused eyelids called a spectacle Nasolacrimal i. Single inferior lacrimal puncta ii. Tortuous nasolacrimal duct with narrowing Uvea i. Birds & reptiles 1. Iris has striated muscle 2. Topical mydriatics not effective 3. Birds- no consensual PLRs Retina i. Birds- pecten ii. Reptiles- conus papillaris 4. Differentiate common ocular disorders occurring in typical exotic pet species Retrobulbar abscess i. Clinical signs: exophthalmos, corneal ulceration ii. Tx: removal of infected tooth, enucleation (caution), flushing +/- antimicrobial impregnated beads  Retained spectacle i. Often environmental ii. Generalized skin disease iii. Systemic illness iv. Injury to spectacle v. Tx: conservative management best Bullous spectaculopathy i. Proximal opening of nasolacrimal duct in subspectacular space ii. Results in fluid accumulation: stomatitis, local tumors or granulomas, trauma, congenital malformation iii. Tx: treat underlying cause, partial speculectomy, recurrence is common Subspectacular abscess i. Ascending infection from oral cavity, penetrating injuries, systemic infections ii. Corneal perforation and panophthalmitis possible sequelae iii. Diagnosis: cytology, culture/sensitivity iv. Tx: treat underlying cause, partial speculectomy, flush with abx, topical/systemic abx Chlamydophila psittaci i. Diagnosis: cytology, IFA, ELISA, PCR ii. Tx: tetracyclines, treat entire aviary Avian poxvirus i. Mosquito vector most common ii. 2 primary forms of dz 1. Cutaneous: featherless skin 2. Diphtheritic- oral & respiratory mucosa iii. Diagnostics: hitopath, virus isolation, PCR iv. Tx: supportive, quarantine affected animals Scaly face mite- Knemidokiptes pilae i. Budgies & canaries ii. Clinical Signs: proliferative, scaly lesions iii. Diagnosis: skin scraping iv. Tx: ivermectin Hypovitaminosis A i. Squamous metaplasia of orbital glands and ducts  ii. Ocular signs: blepharitis & conjunctivitis, secondary bacterial infections common iii. Poor nutrition iv. Most common in avian & chelonian species Hypovitaminosis C (scurvy) i. Susceptible to vitamin C deficiency ii. Conjunctivitis iii. Require supplementation Treponema cuniculi i. Lesions on vulva, prepuce, eyelids, lips, nares, anus – flare up with stress ii. Diagnosis: histopath, skin scrape iii. Tx: penicillin injections Dacryocystitis i. Inflammation of nasolacrimal system ii. Clinical signs: purulent ocular discharge, conjunctival hyperemia, medial canthal dermatitis iii. Tx: address underlying cause, nasolacrimal flush, topical antibiotic solution, systemic antibiotics, recurrences are common Osseous metaplasia i. Metaplasia of ciliary body ii. May lead to secondary glaucoma Encephalitozoon cuniculi i. Dwarf rabbits- transmitted in urine ii. Infects the lens during development iii. Can results in lens capsule rupture Topic: Food Animal Ophthalmology 1. Develop an accurate differential diagnosis list when presented with an animal with corneal opacity Acute IBK o Epiphora, conjunctivitis o Photophobia, blepharospasm o Corneal edema Subacute IBK o Keratitis  o Central corneal opacification -> ulceration Chronic o Severe keratoconjunctivitis o Ocular rupture 2. Using information gathered from a history and physical exam be able to differentiate between and rank in order of likelihood the common causes of corneal opacity 3. Recommend an appropriate treatment protocol for infectious bovine keratoconjunctivitis (IBK) keeping in mind the issue of ELDU and the utility of non- antimicrobial therapies Topical o Erythromycin, tylosin, ampicillin, bacitracin, neomycin, oxytetracycline, penicillin o Requires ELDU Subconjunctival medication o Administer penicillin in the dorsal bulbar conjunctiva o Requires ELDU Systemic o Oxytetracycline, tulathromycin o Does not require ELDU Patches, third eyelid flap, tarsorrhaphy 4. Recommend management strategies to help prevent and/or manage outbreaks of IBK Protection from environment o Shade, dust, fly control, separation of affected animals Vaccination o Best luck with autogenous 5. Recognize the various stages of Bovine Ocular Squamous Cell Carcinoma (BOSCC) Premalignant tumors o Small, white elevated plaques o Papilloma-like structures Malignant tumors o Irregular, nodular, pink, erosive o Become necrotic as tumor outgrows blood supply Common locations o Lateral limbus, eyelid margins (especially lower eyelid), nictitans (third eyelid), medial canthus 6. List the treatment options for BOSCC  Radiofrequency hyperthermia Cryotherapy Surgical removal Laser therapy Immune therapy 7. Recommend an appropriate treatment for the various stages of BOSCC 8. List the options for providing ocular anesthesia to facilitate examination and/or treatment of BOSCC in a standing animal including awareness of the pros and cons of each approach Topical o Cornea: proparacaine o Xylocaine HCL: suppresses mitosis, reduces blink reflexes Auriculopalpebral nerve block o Branch of facial n. o Motor only Line block o Anesthesia of lid Peterson eye block o Indications: enucleation, dehorning, trephination of sinuses, eye sx o Blocks oculomotor, trochlear, abducens, 3 branches of trigeminal Retrobulbar block o Blocks eye and assoc. Structures innervated by 1. Optic, oculomotor, trigeminal, abducens, and facial nerve 9. Develop an accurate differential diagnosis list for a small ruminant with ocular disease Mycoplasma keratoconjunctivitis Chlamydial keratoconjunctivitis Final Review Session PLRs o Mass on optic nerve: afferent ▪ Consensual: negative o Tumor at optic chiasm ▪ PLR: negative OU PLR & vision pathway o Optic nerve and retina = vision o Ciliary ganglion= not involved in visual pathway  o Cortex= PLRs normal- no pathway extends to cortex Horner’s syndrome is a lack of sympathetic innervation to the eye; therefore pupil size is expected to be miotic. o Ptosis of eyelid, enophthalmos, nictitating membrane elevated Globe proptosis o Remove eye OR Replace globe into eye o Prognosis for vision is poor to grave o Medial rectus always the first muscle to tear Exam Techniques o Normal diagnostic values ▪ STT, IOP, etc. o Stroma= hydrophilic o Ulcer= no epithelial cells Epiphora o Tearing o Pain, obstruction of duct Dry eye o Autoimmune disease o Cyclosporine o Dry ipsilateral nostril o Long-acting otic meds o Sequelae: ulcers, pain, vision loss, conjunctivitis o Pilocarpine? Entropion o Primary vs spastic ▪ Proparacaine ▪ Spastic- entropion should resolve with proparacaine ▪ Temporary tacking ▪ Permanent procedure? o Sequelae: Ulcers Anatomy o Cornea 4 layers: epithelial cell layer, stroma, endothelial aspect, Descemet's membrane o Cornea clarity: avascular, endothelial pumps (Na/ATPase)- aqueous humor out of stroma, unmyelinated nerves  ▪ Healthy cornea= aqueous humor + tear film Blue eye o Glaucoma, uveitis, lens luxation, endothelial cell abnormalities Corneal ulcers o Trauma, ectopic cilia, foreign body o Superficial, non-infected corneal ulcer treatment ▪ Topical abx (neo-polybac) ▪ Atropine ▪ Systemic pain med (carprofen, meloxicam) ▪ E-collar o Infection makes worse ▪ Corneal cellularity ▪ Keratomalacia ▪ Stromal ulcer ▪ Severe reflex uveitis o SCCED (indolent ulcers) ▪ Non-healing superficial ulcer o GSD- pannus- chronic superficial keratitis ▪ Cyclosporine- maintenance therapy ▪ Topical steroid Uveal tract o 3 parts: ciliary body, iris, choroid o Nutrients to eye (vascular tunic), aqueous humor, blood ocular barriers Etiologies of uveitis o Ocular ▪ Dog- reflex uveitis- corneal ulcer led to inflammation ▪ Cat- reflex uveitis- herpesvirus ▪ Horse- fungus in corneal ulcer, stromal abscess o Systemic ▪ Dog- lymphoma ▪ Cat- FIP ▪ Horse- septic foal ▪ Uveodermatologic syndrome Tapetum- choroid o Chorioretinitis -> hypo reflectivity o Degeneration -> hyperreflectivity ▪ Shining through less tissue  Retinal detachment o Rhegmatogenous – tear ▪ Refer o Non-rhegmatogenous - no tear Reflex uveitis- corneal ulcer o Horse- atropine, antifungals Retinal diagnostics o Ocular U/S - retinal detachment suspected o Electroretinogram- SARDS Cataracts o Genetics o Diabetes o Sequelae: uveitis Glaucoma o Acute vs chronic ▪ Bupthalamos ▪ Blue- corneal edema ▪ Blind- both Reversible or non-reversible Contraindications o Corneal ulcer drugs- topical steroids or NSAID o Dilate pupil- lens instability, glaucoma o Retropulsion of the globe-