Exam 4 Flashcards

1
Q

Lecture 1 Ophthalmic Examination

A

Squinting: Blepharospasm
Night blindness: Nyctalopia

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2
Q

Design an orderly examination that fulfills the minimum ophthalmic database for a companion animal with a red, cloudy eye

What happens to tear production, IOP, pupils, eye and 3rd eyelid when sedatives are administered?

Why should you decrease the intensity of bright light during exam?

A

Essential Equipment

-Bright focal light source
-Means of magnification
-Ophthalmoscope for fundus (direct, indirect) examination
-Tonometer

Ancillary Diagnostic Materials

-Sterile culture swabs
-Schirmer tear test strips
-Fluorescein dye test strips
-Proparacaine HCl for topical anesthesia
-Tropicamide (1%) for short duration dilation pupils
-Sterile ophthalmic irrigating solution or saline

Optional Equipment

-Slit lamp biomicroscope
-Cobalt blue filter
-Kimura platinum spatula/cytology brush
-23-25 g nasolacrimal cannula
-Dressing forceps

The basic examination

  1. Signalment
  2. List of breed-related ocular abnormalities OFA.org
  3. Ocular and medical history
  4. Previous ocular meds or treatments
    -Drug-related changes can be recognized
    -Reduced likelihood of repeating unsuccessful treatment
  5. Evaluate patient’s temperament before dimming the lights
  6. Perform exam without sedation if possible. Sedatives = eye sink backward, third eyelid protrudes, pupil constricts, both tear production and IOP decrease.
  7. Decrease bright light source intensity, painful eye conditions increases sensitivity to light
  8. Use retroillumination technique to asses clarity of cornea and lens.
  9. Presence of PLR does not = vision

Minimum Ophthalmic database

  • Palpebral reflex
    -Menace response
    -Direct and consensual pupillary light reflexes
    -Dazzle reflex
    -Schirmer tear test
    -Fluorescein dye test
    -Tonometry

Systemic examination

Distance assessment

-Mental status and posture. Blind: head down, move cautiously
-Look for signs of discomfort: squinting, tearing, prominence of 3rd eyelid.
-Ocular discharge if present, character, color.
-Size, position and mobility of eyes.
-Periocular swelling or deviation of the eye’s alignment
-Globe-orbit relationship both eyes compared from above
-Facial or generalized dermatologic disease present?

If no discharge or overt ulcer

-Neuro ophthalmic testing
-PLR: abnormalities such as iris atrophy, adhesions, lens dislocation, elevated IOP, drugs, anxiety. PLR presence does not = vision (central) vs. reflex subcortical. Speed and degree of pupillary constriction Ex: the indirect PLR OS to OD is present or positive.
-Menace response: crude test of vision . Normal response is to close the eye or blinking. Test of afferent tract, retina, optic nerve, optic chasm, optic tracts, lateral geniculate nucleus and optic radiations to visual cortex. CN VII relays information, learned response not reflex.
-Oculocephalic reflexes: Patient’s head taken through various positions and the globe’s position observed, neck flexed, neck extended, normal horizontal nystagmus. Failure indicates dysfunction of central or peripheral vestibular system.
-Dazzle reflex: is a subcortical reaction that complements the PLR and menace response. Shining a bright light to cause a quick squint the eye closed. No vision assessment. Implies functional retina/optic nerve and supports aggressive methods such as surgery to save the eye.
-Maze test: Good to assess vision in dogs, not reliable in cats. Obstacles placed in room or cotton balls dropped to assess visual tracking.
Follow order begin externally and ends with evaluation of the fundus

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3
Q

Red eyed & Cloudy eyed exam

A

Red eye

Should have tonometry performed prior dilation of the eyes

-Note eyelid discoloration, swelling, or loss of hair
-Inverted or everted margins?
-Extra eyelashes on margin?
-Meibomian glands abnormalities
-Size of eyelids, can animal fully open them?
-Assess third eyelid position
-Assess conjunctiva for increased redness secondary to inflammation or loss of color suggesting anemia
-Check for swelling, hemorrhage, follicle formation, foreign bodies, or tumors

Cloudy eye

Glaucoma and lens instability are contraindications for pupillary dilation

-Check for loss of clarity or contour
-Loss of transparency can occur with edema, white blood cell accumulation, cholesterol or mineral deposits, pigmentation, scarring, or vascularization.
-Blood vessels should be categorized by depth. Superficial arise with chronic surface disease, deep more often indicate IOP disease.
-Superficial vessels: originate in conjunctiva, can be seen crossing the limbus from ciliary vessels in the sclera. They have a short, “paint brush” appearance, encircle the cornea perimeter.
-Changes in corneal contour are most often a consequence of ulceration, pronounced edema, enzymatic destruction, etc.
-Color, depth and clarity of anterior chamber fluid can indicate shifts in position of lens, or change in thickness or iris, or IOP inflammation. INCREASE in aqueous humor PROTEIN or CELLS
-Constricted pupils are indication of inflammation
-Dilated pupils are indication of neurological abnormalities, increased IOP (glaucoma), age-related iris thinning, topical drug effects, and fear.

Clarity of lens

-Cataracts of the lens occur in dogs of any age, less common in cats
-Assessment of the fundus reflex is the simplest means of evaluating the clarity of the lens.
-Direct ophthalmoscope on 0 diopters 12-18 inches from eye and view the light reflected from fundus.
-Normal fundus: regardless of color should be uniform throughout the pupil and free of aberrations

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4
Q

Recommend and Defend the selection of a topical pharmacologic agent routinely used in the ophthalmic examination to dilate the pupil for fundus evaluation and anesthetize the ocular surface for tonometry

A

1% Tropicamide
-After 2 applications 5 minutes apart produces maximum dilation
-OA: 20 minutes
-DOA: 4-6 hours

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5
Q

Explain why atropine is undesirable as a mydriatic in the ophthalmic exam

A

Topical Atropine

-Requires 45 minutes to take effect
-Dilation lasts days

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6
Q

Explain the diagnostic importance of the dazzle reflex and menace response in a diseased eye

A

-Dazzle reflex: is a subcortical reaction that complements the PLR and menace response. Shining a bright light to cause a quick squint the eye closed. No vision assessment. Implies functional retina/optic nerve and supports aggressive methods such as surgery to save the eye.

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7
Q

Predict the undesirable effects of general anesthesia that complicate the ocular examination or alter ancillary test results

A

-Increased parasympathetic tone
-Reflexes reduced
-Things that can not be assessed accurately: reflexes, responses, vision, pupil size, globe movement and position, Schirmer test (STT) value, etc.
-Globe becomes exophthalmic and rolls ventrally, impossible examination

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8
Q

Describe the technique and diagnostic benefits of retroillumination

A

-Direct ophthalmoscope on 0 diopters 12-18 inches from eye and view the light reflected from fundus.
-Normal fundus: regardless of color should be uniform throughout the pupil and free of aberrations
-Provides accurate estimate of amount of light reaching the retina and a reasonable prediction of the expected quality of sight.
-Can also compare pupil size/symmetry
-Fundus reflex can also be used to pinpoint a cataract’s location based on the directional movement of the opacity.
-Centrally stationary opacities = located in the nucleus
-Opposite in direction of globe movement = are in posterior lens

Indirect Fundus Exam

-Image upside down and backwards
-At arms length

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9
Q

Predict the PLR, menace response and dazzle reflex in a patient with a facial nerve deficit and a cortically (centrally) blind animal

A

-No closing of the eyelid
-Centrally blind = no menace response present

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10
Q

Explain why a Schirmer tear test is performed prior to pupillary dilation or fluorescein dye application

A

-Performed before any diagnostic drops or medication are applied to the eye step 1.
-If the corneal surface is cloudy and the eye is painful, a fluorescein dye test may be performed as step 2.
-Postpone fluorescein dye test if need to examine retina to ensure clear view of fundus
-If IOP glaucoma suspected, then assess pressure as step 3

The Scheirmer test

-Use to assess tear production (normal >15mm/min)
-Notched end of the prepackaged sterile strip is placed over the lower eyelid into conjunctival sac
-Close eyes, wait 1 min
-Normal values >21 +/- 4.2SD mm/min Dogs, Cats >16.2..

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11
Q

Explain Physiologic basis of the fluorescein dye test and what a positive test indicates

A

Fluorescein dye test

-Use to determine the presence of corneal ulcer and is indicated in any red eye, painful eye with irregular corneal surfaces
-One or two drops of sterile eyewash are applied to the strip
-Dye is applied to the dorsal sclera of the eye. Avoid touching the eye as it can result in a false result area
-Excess stain is irrigated from the eye with sterile saline
-Cobalt blue light is used to detect retention of dye, corneal ulcer retains dye.
Normal hydrophobic epithelium would repel dye = negative result

Positive test, corneal ulcer = hydrophilic stroma retains the dye
-Nasolacrimal duct patency can be tested with dye
-Jones test: let dye come out at nasal duct exit 1-5 minutes
. If not out, check inside the mouth in pharynx
-Flush if blocked, optic anesthetic

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12
Q

Identify a diagnostic test that evaluates tear quality rather than tear quantity and how that test is performed

A

Tear Film Stability by Measuring Tear Film Break-up Time

-After application of dye, manually blink to distribute dye
-Blue light source 15-20 seconds normal, less abnormal

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13
Q

Tonometry, Cytology

A

-Measurement of IOP
-Red painful eye
-Screening for glaucoma
-Cocker Spaniel, Basset Hound
-Uveitis and glaucoma
-Normal range 8-25 mmHg
-No more than 20% difference in eyes
-Anesthetized corneal surface

Cytology

-Ophthalmic bacterial culture for rapidly progressing corneal ulcers
-Poorly healing ulcers
-Anesthetic, cytology brush conjunctival surface

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14
Q

Lecture 2

A

Eyelid disease is common in dogs,
not frequent in cats

Skull conformation, orbital contents, characteristics of the skin, considered desirable facial features in certain breeds, no singular genetic component in eyelid disease

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15
Q

Consequences of Uncorrected eyelid agenesis in the cat

A

Eyelid Agenesis

-Failure of development of a portion of the eyelid
-Almost exclusively seen in the cat
-Persian breed affected most
Superior temporal eyelid typically affected
-Minor defects may be asymptomatic
-Severe agenesis results in corneal and conjunctival exposure and contact with facial hair, increased lacrimation, secondary corneal disease

Tx
-Cryosurgery: eliminates hairs
-Entropion procedure to evert the adjacent cilia.
-Larger defects a pedicle graft from the lower eyelid or adjacent facial skin is indicated.
Common post-operative complication with grafts is misdirected hairs
-Lip to lid transposition provides more natural mucocutaneous margin, hairless border created

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16
Q

Clinical signs that necessitate treatment of distichiasis

A

-Abnormality where the eye lash originates from the meibomian gland
-Meibomian glands: secret lipids that form the superficial layer of tear film to protect evaporation of the aqueous phase.

C/S

-Tearing
-Squinting
-Corneal disease: scarring, pigmentation, ulceration

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17
Q

Compare Entropion pathology and surgical correction in dog and cat

A

Pathology

-Inversion or “in-rolling” of the eyelid margin
-Relatively common in the dog
-Developmental, breed-related disorder commonly
-Cicatricial entropion: chronic inflammatory disease
-Spastic entropion: painful ocular disease FELINE mostly
-Surgery should not be delayed if cornea has been damaged
-Dx: schirmer tear test, fluorescein dye test. 0.5% Proparacaine to eliminate corneal sensation so that anatomical and spastic components can be differentiated. Failure to make distinction can lead to surgical overcorrection

Eyelid tacking

-Temporary correction of anatomical entropion in puppies
-Can be used in older dogs for relief of spastic entropion
-The older the animal is when tacking is performed, the less likely it would resolve the entropion without additional surgery
-Procedure: 2-4 vertical mattress sutures in the affected lid 5-0 nylon 2mm from margin do not place suture through the margin

Tissue excision

-Hotz-Celsus Procedure
-Everting the lid margin by removing the elliptical segment of eyelid skin equal to the degree of inversion.
-Certain details increase surgical success
-Incision 2mm from margin
-#15 blade
-Undercorrection with the need for a second operation is preferable to overcorrection that results in cicatricial entropion
-Rottwilers and Retrievers with upper and lower entropion combined with lateral cantonal laxity required modified technique
-SharPei and Chows challenging due to facial skin folds
-Some cats ha minimal lid laxity, classical Hotz-Celsus procedure usually is effective
Eyelid spasms may persists after surgery, chronic herpetic keratoconjunctivitis

-Injectable collagen filler have been used in recent years to correct mild entropion in young and adult dogs and cats

Ectropion

-Eversion of the eyelid
-Less common to required surgical correction
-Secondary conjunctivitis can be controlled medically with lubrication ointment and intermittent steroids
-V-resection procedure for correction near the lateral canthus. Excise the portion of the eyelid that overlaps the lateral side of the wound.

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18
Q

Macroblepharon

A

-Breed related exophthalmos
-Risk factor for corneal ulceration in brachycephalic breeds

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19
Q

Most common eyelid neoplasm in dog and cat, describe appropriate course of action

A

Dogs

-Most are benign, slow-growing, non-irritating: do not need to be excised unless they threaten to compromise the lacrimal punctum
-Most common is the meibomian adenoma
-Mast cell tumors worst prognosis

Cats

-Almost always malignant
-Should be removed at the earliest possible opportunity
-Most common is squamous cell carcinoma
-Mast cell tumors usually benign

Tx

-Complete surgical excision recommended in most cases
-En bloc surgical resection
-Preserve as much of the eyelid margin as possible
-Four-sided technique instead of V or wedge resection
-S full thickness, parallel cuts perpendicular to margin, 1-2mm on either side of the mass, and extend as needed.
-Connect the distal ends with a V-shaped incision adding the “roof” to the sides of the “house”
-Close using two layers
-Submit tissue in 10% formalin for histopath

Cryosurgery

-May be preferred if mass impinges on a lacrimal punctum
-Nitrous oxide probe temp -196C.
-Chalazion forceps to impede blood flow to the site (Chalazia is a non neoplastic enlargement of the meibomian gland caused by blockage of its duct)
-Double-freeze technique and slow thaw
Cryosurgery specially useful for older debilitated patients
-Can be performed with sedation and local anesthesia

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20
Q

Briefly detail surgical repair of full-thickness eyelid laceration involving the middle section of the inferior eyelid, tissue layers and reconstruction plan

A

-Most lacerations occur perpendicular to the eyelid margin
-Rich vasculature of the eyelid promotes rapid healing
Always assess the entire eye for signs of injury
Avoid excision of flaps that involve the lid margin
-Close all traumatic lacerations in 2 layers
-Start in the apex of the wound
-Oppose the conjunctival edges 6-0 absorbable suture, simple continuous
-Bury the knots to avoid damage to adjacent cornea
-Reappose margin PERFECTLY with a single 6-0 absorbable suture in a figure-of-eight pattern to prevent cosmetic and malfunction defect
-Simple interrupted skin sutures ~2-3 mm apart
-Systemic and topical antibiotic and NSAIDs for 7 days
-E-collar

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21
Q

Anatomical and functional eyelid abnormalities that threaten corneal health in brachycephalic canine breeds

A

Components of the eyelid

-Skin
-Skeletal and smooth muscle
-Fibrous connective tissue
-Mucous membrane
-Cilia
-Modified sebaceous glands
-Superficial layer
-Deep layer: fibrous tarsus and inner conjunctiva
-Dogs have eyelashes only on the upper eyelid (modification of lid hair often passes for lashes)
-Cats lack eyelashes completely
-Highly vascularized, resistance to microbial infection
-Meibomian glands: 30-40 perpendicular to each eyelid margin opening into marginal furrow
-Upper eyelid more mobile than lower
-Orbicularis oculi muscle major m. responsible for closure. Innervated by the palpebral nerve.

Macroblepharon

-Breed related exolphthalmos
-Corneal ulcerations in brachycephalic
-Exaggerated palpebral fissures
-Prominent eyes combined with excessively large palpebral fissures
-Corneal exposure
-Superficial keratitis (corneal inflammation)
-Recurrent ulcerations
-Crocker spaniels, Bloodhound, St Bernard
-Tx: Excise the lid margin and meibomian glands at the lateral canthus and close the defect in 2 layers as described for lid shortening of entropion. Can be done medially but careful not to damage nasolacrimal puncta and canaliculi in this region. Medial closure has the advantage of resolving concurrent medial entropion medial cantal hairs, and contact by hairs of the facial folds

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22
Q

Blespharitis C/S, treatment plan for Staphylococcal hypersensitivity

A

-Acute eyelid swelling in a young dog is characteristic of the ocular manifestation of juvenile cellulitis/pyoderma (“puppy strangle”)
-Adult: slowly progressive swelling, peri ocular alopecia, excoriation, meibomian gland distention and conjunctivitis.

Staphylococcus aureus
-Hard to culture
-Bacterial hypersensitivity requires systemic antibiotic and corticosteroid for several weeks
-Relapses are common is therapy discontinued prematurely
-Ddx: dermatophytosis, demodecosis, immune-mediated mucocutaneous disorders such as pemphigus, atopy, food allergy, neoplasia, mycosis (cutaneous lymphoma) and allergic reactions to insect stings and medications

Chalazion

Focal eyelid inflammation is termed HORDEOLUM
-Acute abscess of one or more meibomian glands
-Tx: warm compresses, topical and oral antibiotics, short course of corticosteroids
-Chronic lipid granuloma from blockage of gland
-Tx: incision and curettage of inspissated material through the conjunctival surface

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23
Q

Prolapsed third eyelid gland preferred surgical treatment and technique

A

Nicitans gland “cherry eye” Prolapse

-Weakness in the fibrous connective tissue anchoring at the gland’s base
Excision of the gland reduces tear production by 30-40%
-Not advisable excision of the gland

Preferred treatment

-Surgical return gland to its normal position
-Simplest technique is the POCKET TECHNIQUE
-Two curvilinear incisions are made through conjunctiva on the posterior surface of the third eyelid using #15 blade
-2-3mm from the free margin and the second 6-7mm toward the base of the third eyelid
-The ends of the two incisions should NOT meet in order to ensure opening/drainage
-6-0 suture to bring the two edges together simple continuous pattern
-Antibiotics for 2 weeks
-No steroids during early healing period
-Activity is restricted

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24
Q

Third eyelid protrusion common causes and Ddx list

A

Common causes of Protrusion

-Ocular pain
-Reduction in orbital tissue mass due to dehydration or atrophy
-Reduced globe size
-Reduced space-occupying orbital disease
-Facial myositis
-Horner’s syndrome
-Tetanus
-Dysautonomia

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25
Q

Inverted eyelid cartilage identification and post operative complication following repair

A

Eversion of the Third eyelid Cartilage

-Outward curling of the third eyelid cartilage occurs most often in a young, large and giant breed dogs
-Burmese most commonly affected cat
-Can be misinterpreted as gland prolapse
-Tearing and conjunctivitis present
-Tx: surgical excision of the deformed section of cartilage
-Incision in conjunctiva and dissection
-Round up the edges of cartilage to avoid irritation
-Post operative antibiotic ointment q 8 hr for 5-10 days

Recurrence of defect is unlikely, but prolapse of the nicitans gland may follow correction
-Thermal cautery may be used for mild defects

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26
Q

Pathology and removal of third eyelid justification

A
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27
Q

Cilia disorders

A

Distichia

-Hairs that arise from the meibomian gland orifices due to misplaced follicles within the adjacent glands
Their presence does not warrant their removal
-Treatment if tearing, conjunctival irritation or corneal ulceration
-Cryoepilation is the most practical treatment
-Chalazion forceps, nitrous oxide cryoprobe, freeze, thaw, then repeat freeze.
-Topical antibiotic q 8hr for 7-10 days

Ectopic cilia

-Distichia that has erupted through the palpebral conjunctiva of the eyelid
-Discomfort, corneal ulcerations often
-Young classically affected
-Squinting and tearing
-En bloc resection is curative, sparing the margin

Trichiasis

-Normal eyelashes with growth toward the eye
-Contact with ocular surfaces, irritation, ulceration.
-Congenital problem in small breed dogs, brachycephalic
-Cryoepilation is commonly used to destroy the offending follicles
-Surgical eversion of the lid margin can redirect the hairs
-Injectable collagen filler can also be used to restore normal cilia position

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28
Q

Lecture 2 & 4

A

Diseases of the Posterior Segment (Fundus)

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29
Q

Describe the Salient Features of the normal fundus

A

Fundus

-Composite picture formed by the optic nerve head (optic disc, optic papilla), sensory retina, retinal pigmented epithelium, choroid, tapetum and sclera, a picture influenced by the animal’s species, breed, age, and coat color.

Sclera

-White to pale yellow
-Visibility depends on the degree of pigmentation in the overlying chorioid and retinal pigmented epithelium as well as the degree of tapetal development

Choroid

-AKA posterior uvea
-Lies adjacent to the sclera
-Normal choroid vessels should be small and uniform size
-Vessels radiate from the optic papilla in spoke-like fashion
-Choroidal vasculature is rarely a complete barrier to visualization of the underlying sclera
-Degree of pigmentation can normally vary. It can be so pigmented that its vasculature is barely discernible or it may be totally devoid of pigment
-Epithelium pigmentation is determined by the same factors that govern coat pigmentation
-GSD masked, while Husky very visible
-In heavily pigmented breeds, melanin lies interspersed between the large vessels of the choroid

Tapetum

-Layer of reflective cells in the dorsal half of the fundus
-Between the retinal pigmented epithelium (RPE) and the choroid
-Reflectivity is dependent on the cell density, greater in the cat than the dog
-Variations that are important are in extent (size) and degree of development
-The overlying RPE is normally devoid of pigment so that the tapetum can be visualized
-Normally the RPE gradually diminishes as it approaches the tapetum
-The tapetum in turn thickens, results in a gradual change in color at its periphery

Retina

-Consists of 10 layers
-Clinical purpose 2 layers
-Outermost RPE and the neurosensory retina
-Gross separation between the two is known as retinal detachment
-RPE is monolayer lies next to the choroid on the ventral area
-Normal variation in RPE determines if the choroid can be seen
-Adjacent and attached to RPE is the semitransparent neurosensory retina, whose contribution to the normal fundus is the most subtle of all layers
Unlike the choroid and RPE, there are no normal variations to the sensory retina per se, variations of the vessels do occur
-Normally in dog 3-5 major retinal venues that radiate superiorly, nasally, and temporally from optic disc, producing venous circle
-The cat has 3 paired retinal vessels never crossing the surface of the optic disc

Optic disc

-Cats: papilla varies little, being unmyelinated and characteristically circular
-Darker in color than canine optic disc
-Canine: marked variations in myelination and assume many shapes. Located within the tapetal fundus as well but may appear in the non-tapetal fundus of toy breeds

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30
Q

List 5 questions one should answer during examination of the fundus

A
  1. Can I get all parts of the fundus in focus simultaneously?
  2. What is the general tapetal “sheen” over the whole fundus?
  3. Are there any focal areas of unusual coloration within the fundus?
  4. How do the retinal vessels appear?
  5. How does the optic disc appear?
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31
Q

Explain the alterations in fundus anatomy responsible for the following variations or pathology

A
  1. Visualization of choroidal vessels in the tapetal and non-tapetal fundus

-Choroid thinning or thickening response to disease
-Collie eye anomaly: thinning
-Uvea is vascular tunic of the eye: choroidal thickening accompanies inflammation
-Tapetal fundus discoloration and decreased reflectivity = choroid disease
-Subretinal exudates = inflammation, possible detachment

  1. Increased tapetal reflectivity

-Suggest thinning/degeneration of the overlying retina
-Decreased light absorption that accompanies retinal detachment/degeneration allows more light to be reflected back to the examiner from the tapetal surface

  1. Diminished tapetal Reflectivity in active chorioretinitis

-Occurs in active inflammation
-Edema, exudation, retinal detachment

  1. Retinal detachment

-Sensory retina pathology: thinning or thickening
-Retinal thinning: increased fundus reflectivity, fallow inflammatory, toxic and ischemic disease processes.
-Retinal thickening: layers are folded, occurs in developmental disorders, or it may swell due to an influx of inflammatory cells, tumor cells, or fluid.
-Sensory retina may respond to pathology by detachment form RPE. Occurs secondary to almost any ocular disease
. Hypo-reflectivity in the area of detachment along with forward shift in the location of the retinal vessels
-RPE changes are generally limited to affecting pigmentation
-Increase or decrease in pigmentation are seen in hereditary retinal degenerations and secondary to inflammatory disease process.
-Decreases in RPE pigmentation are readily seen in the non-tapetal fundus
-Retinal blood vessels respond by change in size
-Attenuated vessels Ddx: anemia, hypovolemia, retinal degeneration
-Vascular enlargement less common Ddx: IOP disease, inflammation, hyper viscosity.
-Retinal hemorrhage Ddx: systemic hypertension, anemia (pancytopenia) and clotting disorders
-Hypoxic states: pink, lipemia animals or deeper red vessels

  1. Optic disc

-Responds by enlargement or decrease in size
-Congenital or acquired changes
-Numerous causes
-Congenital hypoplesia or acquired optic atrophy following inflammatory disease, trauma or retinal degeneration will reduce the size of the papilla.
-Enlarged papilla, neoplasia, inflammation or edema

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32
Q

Summarize and recognize the clinical features (including breed disposition, congenital or adult onset, type of inheritance, presenting history, and likelihood of progression) of the following inherited disorders

A
  1. Collie eye anomaly

-Posterior segment abnormalities
-Collie breed 80-85% affected
-Autosomal Recessive
-Shelter, Border Collie, Australian shepherd also have a congenital ocular anomaly similar to that of the Collie, but much low prevalence.
-Diagnosed by 8 weeks of age
-Bilateral ophthalmoscopic lesions, progressive and increasing in severity.

C/S
-Choroidal hypoplasia (pale area temporal to the optic disc)
-Optic nerve and Scleral Colobomas
-Retinal detachment/hemorrhage
Choroidal hypoplasia is the most common lesion encountered
-DNA test available

  1. Retinal dysplasia

-Embryologic developmental abnormality
-Retinal layers are variably disorganized
-The more severe dysplasia manifests as detachment or non-attachment.
-Inherited from uterine infection (canine herpesvirus, feline panleukopenia)
-Dx by 8 weeks of age
-Many breed affected
Uncommon in the cat
English Springer Spaniel: autosomal recessive trait
-Bedlington, American Cocker Spaniel, etc.

C/S
-Bilateral non-progressive, multifocal lesions appear as round or linear areas of discoloration in the tapetal fundus.
-Lesions appear as hyper-reflective as the tapetum matures
-Centers are pigmented

Functional vision is spared
-Blindness results when retinal tears or detachment accompany severe retinal disorganization

-Cataracts in the Springer possible
-Labradors, multifocal folds within the tapetal fundus.
-Retinal detachment, corneal opacification, cataracts, vitreous degeneration, glaucoma (COL9A3 gene)
-Short limb dwarfism
Samoyed: skeletal dysplasia also present

  1. Optic nerve hypoplasia
  2. Generalized PRA (progressive retinal atrophy)

-Inherited retinal degeneration in a variety of breeds 86 breeds reported

C/S
-Initial night blindness (nyctalopia) that progresses to total blindness
-Older animals more common
-Blindness < 1yo: Collie, Irish Otter, Cardigan Welsh corgi
-Slower progression, blindness > 1yo: Gordon setter, Dachshund, Akita, Miniature schnauzer, Norwegian elkhound, Tibetan terrier.
-Late onset, slow progression, Onset >2yo, Blindness 4+ yo: everything else, Golden retriever, Poodle, etc.

Cats

-Abyssinian: early onset, inherited autosomal dominant trait, onset 8-12 weeks old, blindness <1 yo. Also, can be late onset 4-6 yo blindness
-Persian and Siamese also affected.

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33
Q

Identify causes on non-inheritable retinal atrophy in the dog and cat

A

-Enrofloxacin in cats 5-20 mg/kg dose
-Defect in transport protein causes accumulation of photo reactive fluroquinolones in the retina, exposure to UVA light = destructive free radicals and rapid retinal degeneration.
-Risk: geriatric, hepatic or renal disease cats.

C/S
-Sudden loss of vision
-Dilated pupils
-Effect within a few days

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34
Q

Describe the signalment, ocular signs, treatment and prognosis in a cat with hypertensive retinopathy

A

-Systemic hypertension in cats
-Systolic BP >180 mmHg
>10 years old
-Sudden or progressive blindness
-Abnormal pupillary light reflex
-Bilateral retinal detachment
-Intra ocular hemorrhage

Dogs
-Hypertensive
-Multifocal retinal hemorrhages

Treatment
-Amlodipine besylate daily
-Can result in retinal re-attachment and return to vision in the cat

Prognosis
-The more chronic detachment the less likely return of vision
-Risk of secondary glaucoma due to hemorrhage

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35
Q

Discuss differential diagnoses for acute vision loss in a middle-aged mixed breed dog with clear eyes, dilated pupils, and poor or absent pupillary reflex

A

SARD (Sudden acquired retinal degeneration)

-Second most common, PRA is most common
-Not reported in cats
-Signalment: middle to older age. Females over represented.
Dachshunds and Schnauzer most represented breeds

C/S
-Acute vision loss without signs of inflammation or discomfort
-Unexplained mechanism
-Loss of photoreceptor outer segments and abnormalities in the nuclear layer
-No obvious fundic abnormalities initially
-First observed 4-8 weeks after onset of blindness, subtle variation in tapetal reflectivity and retinal vessel segmentation
-PU/PD, polyphagia, weight gain, panting consistent with Hyperadrenocorticism
-Acute vision loss, abnormal pupillary reflex, optic neuritis
-Normal PLR with cortical blindness
Electroretinography for definitive dx

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36
Q

List 3 causes of Chorioretinitis in the dog and cat

A

Suggestive of systemic disease
-Infectious and/or neoplastic causes
-Prognosis for vision is guarded

  1. Viral: Distemper, Cat: FIP, FLV, FIV.
  2. Bacterial: Brucellosis, Borreliosis, Cat: Bartonellosis, Tuberculosis
  3. Fungal: Cat and dog: Blastomycosis, Cryptococcosis, Histoplasmosis, Coccidioidomycosis, Aspergillosis
  4. Parasitic: Toxocara canis migrating larvae, Cat: Toxoplasma
  5. Neoplastic: Lymphosarcoma, multiple myeloma, metastatic neoplasia

-Optic neuritis: appears swollen and indistinct
-Inflammation of the posterior segment
Unless vision is affected or other ocular tissue is concurrently inflamed the eye may appear unremarkable until ophthalmoscopic exam

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37
Q

Describe the funduscopic features that differentiate active from inactive chorioretinitis

A

Active Chorioretinitis

-Tapetal fundus hazy and gray
-Edema, exudates may obscure tapetal reflection
-Non tapetum area, edema and exudates appear gray or white obscuring RPE and choroid
-Retinal vessels may appear hazy due to perivascular cellular cuffing
-Hemorrhage may be present at various tissue levels
-Retinal detachment may occur secondary to inflammation and or choroidal exudates

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38
Q

Identify 2 congenital disorders of the fundus that could limit vision in a puppy

A
  1. Canine Multifocal Retinopathy
    -Mastiff, Bullmastiffs, others
    -Early onset disease
    3-6 months of age onset
    -C/S: acute, multifocal, serous retinal and RPE detachment.
    -Circular and gray-tan lesion. May regress, remain stationary or progress to degeneration
  2. Acquired retinopathies

-Chorioretinitis or posterior uveitis: Canine distemper virus infection

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39
Q

Describe the near-ophthalmic exam findings characteristic of optic neuritis, its treatment and prognosis for vision

A

Optic neuritis

-Swollen, indistinct optic disc, poorly defined margins, adjacent retinal hemorrhage and detachment.
-If only the retrobulbar portion is affected, there may not be observable changes in the optic disc itself
-Vision loss is typically acute
-Affected pupils are widely dilated and PLR are absent or often delayed
-Granulomatous Meningoencephalitis association
-Ocular trauma, neoplasia
-Most cases are idiopathic or immune-mediated
-Less common in the cat

Treatment
-In the absence of an etiologic diagnosis: immunosuppressive corticoids for 14 days , tapered gradually until maintenance dose is determined
-Alternatively immunosuppressive agents (azathioprine, cyclosporine) may be substituted
-Prognosis for vision is poor, optic nerve atrophy sequela common

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40
Q

Lecture 5

A

Disorders of the Lacrimal system

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41
Q

Identify causes of inadequate tear production

A

Iatrogenic causes

-Etodolac, galliprant, various sulfa drugs, atropine
-Surgical excision of nictitans gland “cherry eye” treatment

Congenital
-Immune mediated disease

Infectious agents

Toxic agents

Neurologic reasons

Inflammatory

Functional Anatomy

-3 layers
-Mucin layer produced by conjunctival goblet cells
-Tear film nourishes cornea and conjunctiva, lysosomes and immunoglobulins, lubrication
-Blinking directs tears to medial canthus, collected in lacrimal lake, capillary action and passive pump mechanism leads to lacrimal puncta
-Drain into a short caniculus, then lacrimal sac, then the nasolacrimal duct.
-Epiphora: tear over production/flow

  1. Deficiency in tear production
  2. Tear excess
  3. Abnormalities within the tear drainage system
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42
Q

Identify the distinguishing features of neurogenic sicca and how its treatment differs from immune-mediated dry eye

A

-Loss of parasympathetic innervation
-Dry nasal purulent discharge
-Complete cessation of tear production

C/S
-Corneal ulceration
-Often herpes virus infection
-Nasal discharge is uncommon for a dry-eye dog
-Ipsilateral dry nostril (XEROMYCTERIA)
-Dry purulent discharge
-Middle age females over represented
Otitis media/interna, trauma or surgery to the ear can be implicated

Treatment

-Oral pilocarpine q6-8 hrs until return of normal production, then maintenance

Feline sicca
-Feline herpes virus implication

43
Q

Describe the effect of inadequate tear production on the canine ocular surface and design a treatment plan to counteract the changes

A

Keratoconjunctivitis Sicca (KCS)

-Syndrome of progressive inflammation and degeneration of the cornea and conjunctiva resulting from inadequate tear production
-Breed-related KCS is attributed to local immune mediated disease of the lacrimal glands, but congenital anomalies, infectious agents, and toxic, neurologic, inflammatory, and iatrogenic factors are all possibilities

Hallmark of KCS is the presence of copious mucoid or mucopurulent discharge
-Bacterial overgrowth

Treatment
-Topical antibacterial will eliminate discharge
-Addressing the underlying cause for tear deficiency

C/S
-Dull cornea
-Hyperemic conjunctiva
-Superficial corneal vascularization and pigmentation will progress
-Opacifying the cornea till blindness may occur
-Secondary ulceration possible

Dx
-Schirmer tear test
-Values < 10 SD mm/min is diagnostic (Normal values >21 mm/min dogs, cats >16 mm/min)
-in brachycephalic breeds any values <15 SD mm/min is significant bc they are predisposed

Treatment

-Topical 0.2% cyclosporine and 0.02-0.03% tacrolimus applied BID, initially alone if sufficient
-Antibiotics, topical lubricants, and/or steroids are generally indicated in the initial management
-Neomycin-polymyxin
-B-dexamethasone
-Re evaluate in 6 weeks
-Drugs above suppress immune injury to lacrimal glands
-Artificial tears not equally effective in all patients, trial and error effort
Hyaluronic acid-base preparations are excellent for KCS

Mucin-deficient tear dysfunction
Examples
-I-drop Vet Plus
-Optixcare Plus

-Failure of BID cyclosporine or tacrolimus to improve condition or decrease clinical signs is an indication to substitute a more concentrated form of tear stimulant
-Oral 2% pilocarpine BID

Surgical treatment

-Parotid duct transposition
-Mineral deposition in cornea risk due to difference in composition between saliva and lacrimal fluid
-Palpebral fissure can also be shortened in certain breeds to reduce exposure and drying

44
Q

Identify the components of the nasolacrimal drainage apparatus

A
  1. Secretory
    -Orbital glands
    -Nicitans glands
    -Meibomian glands
    -Conjunctival goblet cells
  2. Distribution
    -Gravity
    -Eyelid blinking
  3. Drainage
    -Nasolacrimal drainage
    -Lacrimal puncta
    -Lacrimal canaliculi
    -Lacrimal sac
    -Nasolacrimal duct
    Lacrimal and maxillary bones to empty via osmium in the ventrolateral floor of the nasal vestibule
45
Q

Describe two methods used to determine patency of the nasolacrimal system

A

Dx
-Application of fluorescein dye to the corneal surface (Jones test)
-Appearance in external nares
-Longer than 4 minutes may be obstruction is present
-Brachycephalics have longer transit times
-If dye does not appear then there is a functional abnormality (e.g., punctual malposition), physical obstruction, or anomalous nasolacrimal opening in the posterior nasal cavity that causes the dye to drain into the nasopharynx rather than nasal cavity

46
Q

Describe silent features of dacryocystitis, C/S, Dx confirmation, one treatment method

A

-Inflammation of the lacrimal sac
-Canaliculi and nasolacrimal duct affected
-Persistent mucopurulent discharge concentrated in medial canthus
-Foreign bodies are common culprits
-Chronic KCS, conjunctivitis, nasolacrimal obstruction are causes
-Bacterial infection involvement

Dx
-Bacterial culture
-Cytology of exudate
-Contrast Dacryocystorhinography
-Radiographs, CT, MRI can help identify foreign body

Therapy
-Relief of obstruction
-Removal of foreign body
-Elimination of infection
-Indwelling catheterization
-Lacrimoscopy and Fluoroscopically guided stunting
-Topical antibiotic solution
-Aqueous corticosteroids for 14-21 dyas

47
Q

Define Epiphora and propose a Dx pan to determine its cause

A

-Abnormal tear flow down the face
-Excessive tearing, obstruction, or tear film mucin deficiency

Cause
-Ocular irritation
-Film mucin deficiency
-IOP disorders such as uveitis

Dx
-Schimer test
-Fluorescein dye test
-TFBUT test

48
Q

Identify and propose a plan to correct a problem of the nasolacrimal punctum that may affect patency in a young dog or cat

A

-If dye does not appear in the external nares and posterior drainage into the pharynx can not be documented, Nasolacrimal flushing is performed

Nasolacrimal flushing

-Topical anesthesia
-The puncta appear as a slit like opening in the conductive located just inside the upper and lower eyelid margins ~5mm temporal to the medial canthus
-The canaliculus then extends toward the medial canthus, parallel to the eyelid margin and just beneath the conjunctiva
-22 g intravenous catheter or stainless steel cannula for nasolacrimal duct can be directed into the punctum
-Sterile saline is flushed through the opposite punctum
-The open punctum is often easier to cannulate since the lid margin can be everted
-Some dogs may swallow which indicates successful passage through a more caudal opening in the nasal cavity
-If the system is patent when flushed, functional cause of epiphora such as entropion and medial cantal trichiasis must be ruled out
-If irrigation is not successful, then duct cannulation with a 0 to 2-0 monofilament nylon or praline may relive or bypass an obstruction
-Cannulation may be maintained for 1-2 weeks by tying the suture material to the facial skin at either end
In many instances epiphora is primarily a cosmetic issue and surgical intervention is optional

Congenitally imperforate puncta and punctual stenosis

-Careful incision with #11 scalpel blade over the punctum or by tenting and excising the overlying conjunctiva with a fine tenotomy scissor

-If cannulation is not successful, extensive surgery may be required
-Dacryocystomaxillorhinostomy
-Orał tetracycline and doxycycline have been used to control facial staining
-Oral Tylosin also used

49
Q

Explain the phenomenon of tear instability and the diagnostic test used to confirm the diagnosis

A

-The tri-laminar film consists of a central aqueous layer sandwiched between outer lipid and inner mucin component
-Premature break up of the tear can lead to dry spots in ocular surface, mimics KCS eventually

C/S
-Ocular discharge
-Frequent blinking
-Rubbing and conjunctival hyperemia
-Cornea changes, roughening and loss of luster
-Subtle superficial vascularization
-Cavalier King Charles Spaniel predisposed

Dx
-Tear film break up time test
-Drop of undiluted fluorescein dye applied to dorsal bulbar conjunctival surface
-Cobalt blue light
-“Holes” appear
-Mucin deficient tear disperse in <5 sec (normal 20 seconds)
-Schirmer test values are usually high

Tx
-Managing concurrent disease that could impact tear components
-Disturbance of meibomian glands, infection, chronic skin disease all may interfere with tear film production/evaporation
-Insufficient production can also reduce film stability
-Chronic or immune mediated conjunctivitis may reduce goblet cell numbers
Cyclosporine or Tacrolimus BID

50
Q

Rationalize use of a tear stimulant in the treatment of epiphora due to a qualitative tear disorder

A

-Cyclosporine
-Tacrolimus
-Hyaluronan-based lubricants

51
Q

Lecture 6 & 7

A

The cornea & Sclera

52
Q
  1. explain the phenomenon of corneal transparency.
A

-4 anatomical layers
-Outer epithelium: hydrophobic
-Stroma: Hydrophilic, lamellae important to clarity
-Descemet’s membrane: innermost endothelium
-Endothelium: one cell thick, hydrophobic, active ATPase pump.

Factors of transparency

  1. Avascular nature, limbal capillaries, tears, aqueous humor
  2. Lamellar arrangement
  3. State of dehydration “deturgescence”
  4. Stroma hydrophilic, sandwiched between lipid barriers to prevent too much fluid
  5. Endothelium regulates aqueous humor influx into the cornea Na/K ATPase pump = corneal clarity.
  6. Hypertonicity of tears drawing fluid away from corneal surface
53
Q
  1. predict a time frame for healing of an uncomplicated epithelial defect that involves 80% of the corneal
    surface.
A

-Corneal surface: 300-400 times density of nerves than skin
-Ophthalmic nerve branch, endings concentrated in the stroma

Epithelium healing

-Outermost layer
-Starts within hours
-Migration, mitosis, maturation = 7 days

Stroma healing

-Irregular fibers
-Keratocytes, leukocytes
-Reorientation 1-2 months
-Infection = scarring, fibroblastic activity, delayed healing, vascularization

Endothelial healing

-Starts within hours
-Descemet’s membrane within 1-2 weeks
-Aging: decrease endothelial function and cell density by 50%

Corneal Response to Disease

-Blue: edema
-Red: vascularization
-Gray: fibrosis or scarring
-Black: melanosis
-Yellow: Stromal infiltration of WBCs
-White: accumulation of lipid or mineral within the cornea

54
Q
  1. differentiate between superficial and deep vascularization of the cornea and the significance of each.
A

Congenital Corneal Abnormalities

Superficial

Dermoid

-Skin-like appendage on cornea/conjuntiva; irritation by associated hairs
-More common in dog (St. Bernard, Dalmatian, Dachshund) than cat (Burmese)
-Surgical excision by superficial keratectomy

PPM-associated Deep Corneal Opacities

  1. Association with persistent pupillary membranes, remnants of embryologic vascular system once covering the anterior lens
  2. Fibrous extend from iris face to inner corneal endothelium
  3. Non-progressive fibrosis, rare intermittent edema
  4. No Tx indicated
  5. Inherited: Basenji, Chow, Pembroke, Mastiff.
55
Q
  1. define a descemetocele and explain its bulls-eye pattern when stained with fluorescein dye.

Deep (stromal) Ulcers

A

Descemetocele: a deep corneal ulcer in which Descent’s membrane is exposed due to complete loss of overlying epithelium and stroma

C/S
-Iris prolapse
-Staphyloma: outward protrusion of weakened corneal tissue, often lined by uveal tissue
-“Melting” appearance to stroma
-Anterior uveitis
-Edema, cellular infiltrates, vessels in cornea
-Non-specific signs of ocular pain

Etiologies
-Failure to identify/correct superficial ulcer
-Infection
-Excess collagenase activity
-Innapropriate corticosteroid therapy

Dx
-“Bull’s eye” pattern on Fluorescein test
-Culture and sensitivity
-Cytology of ulcer margin
-Schirmer test
-Leaking wound: Seidel’s test positive, rivulets of bright green fluorescein dye extending from margin of lesion

Tx
-Direct therapy toward cause
-Correct lid or tear abnormalities that may be contributing
-Neomycin-polymyxin B-bacitracin solution, Cephalosporin compound
-Gentemicin or Tobramycin or Fluoroquinolone (only for most serious cases)
-Cephalosporin combined with amino glycoside or Fluoroquinolone
-Topical autologous serum
-Oral doxycycline
-Tarsorrhaphy temporarily (or third eyelid flap) to prevent drying
-Conjunctival graft if needed > half corneal thickness affected
-Corneal-conjunctival transposition
-Alleviate anterior uveitis: Systemic NSAIDs, 1% Atropine judiciously if mitotic, Topical corticosteroids/NSAIDs contraindicated

56
Q
  1. use an ulcer’s location on the corneal surface to hypothesize its etiology.
A

Ulcerative Keratitis (Corneal Ulceration)

-Loss of epithelium with or without loss of corneal stroma

General Signs

-Blepharospasm (Spasmodic blinking), rubbing at eye, tearing, third eyelid protrusion
-Corneal changes: loss of transparency due to edema, corneal contour changes

Dx

-Fluorescein dye test

Etiology

-Endogenous: lid abnormalities, exposure, inadequate tear volume
-Exogenous: abrasion, foreign body, chemical burn

Complication of healing

-Infection: virus, bacteria, fungus
-Defective epithelial basement membrane
-Excessive collagenase activity: Pseudonyms and Streptococcus produce proteinases “Melts” stroma
-Brachycephalic breeds: produce too much enzyme in response to corneal injury

Superficial Ulcer, Uncomplicated

Location

-Central: lagophthalmos (incomplete closure of the eye), drying
-Ventromedial: nicitans, foreign body
-Dorsal: ectopic cilia
-Ventrolateral: entropion

Tx

-Topical prophylactic antibiotic broad-spectrum
-1% Atropine ointment to dilate pupil during exam
-Elizabeth collar to prevent self-trauma
Avoid topical corticosteroids
-Inhibit migration, mitosis of epithelium
-Decrease stroma fibroblastic proliferation
-Inhibit antimicrobial response
-Potentiate collagenase activity and stroll “melting”
-Re-evaluate in 3-5 days
-If no response to treatment: re-examine for foreign bodies, cytology, bacterial culture, evaluate ulcer margin for epithelial lipping

57
Q
  1. compare and contrast the salient features of a non-healing corneal epithelial defect (erosion) in the dog
    and cat.
A

Superficial Ulcer - Recurrent Epithelial Erosion

Dog

-C/S: Diffusion of fluorescein defect beyond margin or lifting of epithelium at margin of ulcer
-Either sex, BOXER (SCCED) most represented
>5 yo

Etiology
-Epithelium fails to adhere to stroma
-Unknown cause

Tx
-Mechanical debridement of epithelial lip with dry sterile cotton swab
-Stromal polish using “Alger Brush” diamond bur
-Broad-spectrum antibiotic
-Hydrophilic contact lens bandage

Prognosis
-80% heal within 2 weeks
-Recurrence likely
-Keratotomy and repeat debridement may be necessary

Cat

C/S
-Usually adults
-Often precipitated by stress, steroids as for asthma
**Pathognomonic DENDRITES (linear/branching/vermiform) or “geographic” appearance coalesce
-Respiratory signs may appear

Dx
-Pathognomonic dendrites
-Response to antiviral therapy
-History of eye disease
-Laboratory diagnosis are nor dependable

Tx
-Antiviral 1 week past resolution
-Idoxuridine 0.5%, Cidofovir 0.5%, Ganciclovir 0.15%, Famciclovir, oral L-lysine
-Stress reduction

58
Q
  1. describe the clinical appearance of a corneal ulcer complicated by a) sepsis and b) enzymatic tissue
    degradation
A
  1. Sepsis: yellow colored, cellular infiltrates, vascularization
  2. Enzymatic tissue degradation: “melting”
59
Q
  1. develop a diagnostic and therapeutic plan for a brachycephalic dog with a rapidly progressive deep ulcer
    in the central cornea.
A

-Brachycephalic breeds: produce too much enzyme in response to corneal injury

60
Q
  1. specify the features of a lipid dystrophy that differentiate it from calcific degeneration (mineralization).
A

Corneal Lipidosis

C/S
-Crystalline, shiny, refractive “ground glass” appearance
-Often centrally located

Lipid dystrophy

-Bilaterally symmetrical
-Breeds, inherited: Siberian Husky, Collie, Sheltie, Cocker spaniel, Cavalier King Charles spaniel, etc. 62 breeds

Lipid Degeneration

-Unilateral or bilateral
-Slowly progressive
Miniature Schnauzer
-Hyperlipemia, hypothyroidism, failure of fat metabolism (storage disease) association
-Failure of cells to utilize lipids normally, secondary to pannus

Tx
-No specific treatment
-Dietary consideration
-Essential fatty acids
-NSAIDs or corticosteroids if vascularization
-Rarely causes vision loss or discomfort in cases of inheritable dystrophy

Corneal Calcification Degeneration

-Age-related
-Geriatric patients
-Hypercalcemia
-Chronic keratitis

C/S
-Rough, gritty corneal deposits, snags cotton swabs
-Dull, chalky appearance
-Plaques may slough, causing rapidly progressive ulceration in these patients

Tx
-Debridement of superficial plaques with Alger brush
-Topical 2% EDTA ointment to chelate mineral weeks to months process
-Deep ulcers may require grafting to maintain corneal integrity

61
Q
  1. differentiate the pathogenesis and appearance of a corneal sequestrum from that of corneal
    pigmentation/melanosis.
A

Feline Corneal Sequestrum

C/S
-Persians, Himalayans, Burmese most affected
-Discomfort
-Brown or black corneal plaque (not melanin)
-Supreficial vascularization
-Hespes virus infection, chronic ulceration, adnexal abnormalities, medial entropic, lagophthalmos/drying association

Dx
-Fluorescein stain uptake peripheral to sequesrum

Tx
-Spontaneous extrusion of plaque
-Prophylactic antibacterial, antiviral
-Bland lubricants
-If painful, keratectomy to remove necrotic plaque
-Excision followed by conjunctival or corneal graft may discourage recurrence

Pigmentary Keratitis

C/S
-Non-specific corneal ulceration sign
-Superficial pigmentation
-Dogs: Boston terrier, Shih tzu, Pug
-Superficial vascularization +/-
-Association with lagophthalmos, facial folds, medial entropion, tear film instability

Tx
-Surgical correction of adnexal abnormalities, e.g., permanent partial tarsorrhaphy
-Topical Cyclosporine to stabilize tear film
-Topical corticosteroid to reduce vascularization (caution due to existing ulcer risk)
-C/S often slowly progress despite therapy

62
Q
  1. predict the clinical course of chronic superficial keratitis (pannus) in a German shepherd if untreated.
A

> 2yo
-Bilateral always
-Temporal quadrant affected initially, then nasal, inferior, superior.
-Early plasma infiltration, sub epithelial vascularization, pigmentation
-Nictitans infiltration concurrent

Etiology
-Presumed immune mediated
-UV light
-High altitudes
-Fall/spring irritants

Tx
-Control not cure
-1% prednisolone acetate or dexamethasone topical
-4-6x daily for 2 weeks, monitor and then taper
-Topical immune mediator: 0.2% Cyclosporine BID
-Tacrolimus oitnment
-Subconjunctival steroid
-Protection from UV light
-Client education
If untreated progresses to blindness

63
Q
  1. explain why corticosteroids are contraindicated in the treatment of a corneal ulcer
A

Complication of healing

-Infection: virus, bacteria, fungus
-Defective epithelial basement membrane
-Excessive collagenase activity: Pseudonyms and Streptococcus produce proteinases “Melts” stroma
-Reactivation of Herpes virus
-Bacterial opportunistic

64
Q
  1. describe the clinical features of eosinophilic keratitis and a diagnostic test to confirm the disorder.
A

Feline Eosinophilic Keratitis

C/S
-Disconfort
-Pink to flesh colored plaque on corneal surface, temporal quadrant common
-Corneal vascularization

Aberrant immune response, Herpes virus in 75% cases

Dx
-C/S
-Cytology: eosinophils, lymphocytes, plasma cells, mast cells, PMNs.

Tx
-Topical antiviral for herpes virus
-Topical corticosteroid (1% prednisolone, dexamethasone) Avoid if corneal ulcers are present reactivation of virus
-Oral MEGESTROL ACETATE: diabetes potential secondary, mammary hyperplasia/neoplasia
-Triamcinolone SQ
-Client education: controllable, 65% recurrence, seasonal exacerbations

65
Q
  1. identify signs consistent with episcleritis and explain the associated corneal pathology.
A

Disorders of the Sclera

Episcleritis - Nodular or diffuse

-Proliferative keratoconjunctivitis, Collie granuloma
-Presumed immune mediated
-Young-middle age Collies, Cocker spaniels

C/S
-Nodular swelling, temporal limbus with corneal infiltration by lymphocytes, plasma cells, histiocytes, and fibroblasts

Tx
-Topical or intralesional corticosteroid therapy
-Surgical excision or cryotherapy
-Systemic immune modulation with tetracycline/niacinamide
-Prednisone, or Azathioprine in refractory cases

Pathology of Corneal Dystrophy or Degeneration

-Breed disposition: Boston terrier, Chihuahua, etc.
-Non-heritable degeneration
-Endothelium degeneration resulting in progressive corneal edema
-Non painful nearly stage
-Later stage: fluid bullae breaks through epithelium to create punctate ulcers
-Progressive to visual compromise

Tx
-Gundersen-type conjunctival flap in early stages to slow edema progression
-5% NaCl ointment to discourage bullae formation
-If recurrent ulceration, surgical referral, thermokeratoplasty, conjunctival flap
-Transplantation of Descent’s membrane (DSEK) from donor eye shows promise

66
Q

Disorders of the Sclera

A

Scleral Ectasia

-Outward “bowing” of the scleral wall
-Australian shepherds
-Elevated blue-black area in anterior sclera
-Collies: affects sclera surrounding optic disc
-Merled dogs: part of multitude of congenital abnormalities
-No medical or surgical Tx

Epibular Melanoma

-Slow growing tumor, benign, origination from pigmented limbus
-German shepherd, Labrador, Gonden as early as 2yo

67
Q

Lecture 8

A

Disease of the anterior uvea

68
Q
  1. name the components of the uveal tract, describe its musculature and innervation, and explain its
    functions.
A

Uvea: vascular tunic of the eye

Components

-Iris
-Iris sphincter muscle: ring of smooth muscle that encircles the pupil near its margin and results in MIOSIS or constriction of the pupil when stimulated. Innervated by parasympathetic system via terminal branches of the OCULOMOTOR nerve.
-Iris dilator: weaker muscle, radially oriented in the posterior iris, innervated by SYMPATHETIC nerves and causes MYDRIASIS or dilation.
-Ciliary body
-Ciliary body muscle: is poorly developed in domestic animals, limited accommodative ability, PARASYMPATHETIC fibers from OCULOMOTOR nerve.
-Choroid
Disorders of anterior uvea (iris, ciliary body) may represent primary ocular disorder or systemic disease association

Physiology/Function

-Aqueous humor produced by ciliary processes epithelium
-Fluid waste removal, nutritional component to cornea, clarity, exclusion of large protein molecules and cellular components
-Mediation of light amount entering the eye PLR
-Near vision adjustment/accommodation
-Alter shape of lens

69
Q
  1. differentiate a persistent pupillary membrane (PPM) from an inflammatory adhesion.
A

Persistent Pupillary Membrane

-Persistent pupillarymembranes: developmental abnormality in the iris (iris collarette)
-Tissue are remnants of an embryonic vascular system
-Site of origin (iris collarette) helps to differentiate from inflammatory adhesions a.k.a SYNECHIA
-Non-progressive opacities at the site of attachment
-Basenji dog
-No therapy indicated
-Inherited in other breeds, Australian shepherd, Chows
-Heterochromia iridis: normal variation in iris color
-Iris atrophy: acquired problem, aging process, secondary from chronic intraocular disease, or unknown etiology. Ddx in patients with non-reponsive or poorly responsive pupils and dilated
-Iris cysts: fluid-filled vesicles, free-floating. Golden retrievers pigmentary uveitis association. Unwarranted treatment otherwise.

Inflammatory Adhesion - SYNECHIA

-Adhesions of iris to lens = posterior synechia
-Adhesions of iris to cornea = anterior synechia, less common

70
Q
  1. differentiate clinically between an iris cyst and an iris melanoma.
A
71
Q
  1. explain the significance of increased iris pigmentation in a cat.
A
72
Q
  1. identify the clinical signs associated with anterior uveitis and explain the pathophysiology of each
    sign.
  2. explain the pathogenesis of lens-induced uveitis
A

Anterior Uveitis

C/S

-Lacrimation: due to ocular pain
-Blepharospasm: due to ocular pain
-Photophobia: ocular discomfort when movement of the inflamed tissues as part of PLR
-Enolphthalmos (retraction of the globe into the orbit): due to ocular pain
-Lethargy, poor appetite: pronounced ocular pain
-Hyperemia: Ciliary flush (engorgement of episcleral vessels) Conjunctival vessels dilation
-Corneal opacification: edema due to endothelial changes, deep vascularization, keratin precipitates. Cats &laquo_space;Dogs
-Cloudy aqueous: increased protein, leukocytes, hypopyon (in ventral chamber), KP’s deposits on corneal endothelium = keratic precipitates. Turbidity due to increased protein content AQUEOUS FLARE.
-Hypopyon: accumulation on the anterior chamber bottom
-Poorly functional endothelium allows influx of fluid into stroma “paint brush” vessels around corneal circumference
-Bloody = hyphen, blood in anterior chamber
-Fibrin: gray, wispy appearance, can become a round clot
-Lipid-laden aqueous: milky white
-Iris changes: edema, hyperemia, miotic pupil. Due to dilation and increased permeability of the small blood vessels.
-Decreased IOP
-Pupillary constriction or MIOSIS: is a clinical sign of uveitis. Inflammatory mediators and tissue edema causes sluggish pupil. During examination it may not dilate with tropic amide, the sphincter becomes antagonist
-Adhesions in iris: can trap behind the iris causing to bow forward, leading to PAS (peripheral anterior synechia) and altering aqueous outflow by obstruction of the iridocorneal angle and predisposing to IOP (glaucoma).

Inflammation of the ciliary body results in decreased function of its epithelium and a subsequent decrease in aqueous production IOP decreases

Consequences may include

-Catarcts: secondary to synechia
-Toxic lens epithelium, lens laxations due to degeneration of ciliary processes
-Glaucoma
-Hypotonic, non-functional globe, etc.

73
Q
  1. develop a therapeutic plan for treatment of acute idiopathic uveitis in a dog and in a cat, to include 1)
    generic pharmacologic agents, b) rationale for use of each drug, c) route of therapy, d) frequency of
    administration, and e) identification of potential adverse side effects of agents recommended in the
    regimen.
A

Tx

Anti-inflammatory therapy

  1. Corticosteroids
    -1% prednisolone or dexamethasone
    -Subconjunctival administration
    -Systemic therapy
  2. NSAIDs: topicals or systemics caution when ulcers present
    -Carprofen or meloxicam

Mydriatic-Cycloplegic Therapy

  1. Atropine 1%
    -Parasympathetic agent
    -Decreases pain by relaxing bridal and ciliary muscle
    -Prevents adhesion of iris to lens (synechia)
    -Restores vascular permeability to normal
    -1-2 SIB, then decrease to maintain pupillary dilation as necessary
    -Ointment preparation minimizes side effects
    -Side effects: reducing tear production, ileus, predisposes to glaucoma, IOP elevation.
    Contraindicated if glaucoma
    -Tropicamide 1% shorter acting, safer if a must
74
Q
  1. list 3 common exogenous causes of uveitis in the dog and cat.
  2. list 2 common sequela of anterior uveitis that result in blindness.
A

Etiology of Anterior Uveitis

Primary ocular disease: often unilateral. Blunt trauma, infection of extra ocular structures such as corneal ulcer, ocular neoplasia, malignant tumors such as melanoma. Lens-induced uveitis due to immune response to encapsulated protein.
-Phacolytic uveitis: inflammation that leads to cataracts from lens induced uveitis
-Phacoclastic uveitis: cat scratch injuries, traumatic rupture of lens
-Idiopathic disease

Secondary consequence of systemic disease
-Metabolic disorder alters vascular permeability, hyphen or flare
-Hypertension and renal failure, choroid disease
-Metastatic tumors
-Infectious diseases
-Viral: canine adenovirus-1 “hepatitis blue eye”. Feline: FLV, FIP, FIV.
-Bacterial: secondary to pyometra, dental abscessation, osteomyelitis). Lepto, brucellosis, bacterial endocarditis, neonatal septicemia
-Fungal: Blastomycosis, histoplasmosis, etc.
-Parasitic: Aberrant Dirofilaria
-Protozoan: Enrlichiosis and RMSF. Riccketsial disease, doxycycline
-Immune mediated: Akita, Siberian husky, Malamute

Dx
-C/S: red, cloudiness, corneal disease.
-Conjunctivitis
-Glaucoma
-Recognition of redness and cloudiness is more challenging in the cat due to limited visualization of the sclera and a cornea that resists edema
-PE assessment of organ systems

75
Q

Lecture 9

A
76
Q
  1. describe the anatomical regions of the lens.
A
  1. Anterior capsule
  2. Lens epithelium
  3. Anterior cortex
  4. Nucleus
  5. Posterior cortex
  6. Posterios capsule
77
Q
  1. describe the supportive structures that maintain lens position and recognize the consequences of shifts in lens
    position.
A
  1. Vitreous posteriorly
  2. Iris anteriorly
  3. Lens zones circumferentially, extending from ciliary processes to lens equator: ciliary muscles shift lens forward to focus near objects, backward relaxes it, far objects.
78
Q
  1. explain the immunologically privileged nature of lens protein and clinical consequences of lens protein
    leakage.
A

-Lens protein is immunologically privileged due to protection from immune system via semi-permeable capsule
-Minor immune tolerance due to constant leakage of small amounts of lens protein
-Rapid protein leakage (as in diabetics) and or chronic cataracts formation influences permeability and capsule damage leads to immune mediated inflammation

Metabolism

-Glucose from aqueous provides most lens energy requirements
-Anaerobic glycolysis is the major pathway of glucose metabolism

79
Q
  1. explain the mechanism by which the nucleus opacifies in the normal aged lens.
A

Lens Aging

Nuclear sclerosis

-Normal change resulting in increased central lens density
-6yo starts
-Opacity appears translucent, smoky pearl dropped into the center of the lens
-Fundus structures still visible, tapetum reflection still visible
-Best evaluated with retroillumination dilated pupil
-Smooth clear nuclear boundary and clear peripheral cortex can be visualized

80
Q
  1. define and classify a cataract on the basis of age of onset, location in the lens, and degree of maturation.
A

Cataract: opacity of the lens, most commonly inherited abnormality. Cats more common due to chronic uveitis

Age of Onset

  1. Congenital
  2. Juvenile
  3. Senile: 6yo or older

Location

  1. Capsular
  2. Subcapsular
  3. Cortical
  4. Nuclear
  5. Suture-related

Degree of maturation

  1. Incipient
    -Early focal opacity
    -Equatorial vacuoles and lens fibers swelling
  2. Immature
    -More extensive opacity
    -Tapetal reflection still visible
    -Lens swelling, uveitis and leakage may be present
  3. Mature
    -Positive PLR (cataracts alone will not cause loss of PLR)
    -Totally opaque lens
    -Optic nerve healthy
  4. Hypermature
    -Liquefaction produces some degree of cortical clearing
    -Phacolytic uveitis
    -Cortex completely liquified
81
Q
  1. differentiate the clinical appearance of age-related nuclear sclerosis from a pathological cataract.
A

Lens Aging

Nuclear sclerosis

-Normal change resulting in increased central lens density
-6yo starts
-Opacity appears translucent, smoky pearl dropped into the center of the lens
-Fundus structures still visible, tapetum reflection still visible
-Best evaluated with retroillumination dilated pupil
-Smooth clear nuclear boundary and clear peripheral cortex can be visualized

Cataracts

-Obscures tapetal reflection

Etiology

  1. Inherited
  2. Developmental: PPM (Persistent pupillary membranes), PHPV (Persistent hyperplastic primary vitreous)
  3. Traumatic
  4. Metabolic
  5. Toxic
  6. Nutritional
  7. Inflammatory: specially in the cat
  8. Idiopathic
82
Q
  1. explain the mechanism of cataract formation in the diabetic dog.
A

Diabetes mellitus

-Hyperglycemia overwhelms the normal metabolic pathway in the lens
-Production of non-soluble sugar alcohol via aldose reductase pathway creates osmotic gradient with influx of fluid into lens
-Disruption of lens fiber membranes leads to protein precipitation and cataract formation

83
Q
  1. identify clinical features that discourage cataract surgery in the dog.
A

Cataract Surgery = elective procedure

-Major health problems should be addressed prior to surgery
-Complete eye exam to identify ocular diseases that would complicate or obviate the need for cataract surgery for example:

-Keratitis
-Inadequate tear production
-Uveitis
-Glaucoma
-Lens subluxation
-Retinal disease
-Active infection/inflammation (otitis, dermatitis, dental disease, cystitis)

Complications of cataract surgery

-Anterior uveitis
-Ruptured posterior capsule?vitreous herniation
-Hyphema
-Shallow anterior chamber
-Wound dehiscence
-Infection
-Glaucoma
-Retinal detachment

84
Q
  1. explain why a miotic agent is contraindicated in a patient with glaucoma secondary to anterior lens luxation.
A

Lens Displacement

Subluxation
-Remains in patellar fossa
-Some zones remained attached

Luxation
-Complete displacement from patellar fossa
-Anterior or posterior luxation

Miotic agents such as Latanoprost, Pilocarpine, and Demecarium are contraindicated bc they exacerbate the pupillary blockade

85
Q

Lecture 10

A

Diseases of the Orbit

86
Q
  1. Describe the C/S suggestive of space-occupying orbital disease
A

Primary C/S

-Exophthalmos
-Enophthalmos
-Strabismus (involuntary fixed deviation of the globe from its central axis)

Secondary

-Ocular discharge
-Lagophthalmos (inability to completely close the eyelids)
-Conjunctival swelling
-Corneal disease
-Optic nerve dysfunction
-Fundus abnormalities
-Retina hemorrhage, etc.

87
Q
  1. objectively distinguish exophthalmos from buphthalmos.
A

Exophthalmos

-Can be caused by a discrete space-occupying orbital mass, neoplasm, abscess, zygomatic mucocele, or vascular anomaly
-Brachycephalic is breed related normally present

88
Q
  1. differentiate retrobulbar neoplasia from retrobulbar inflammation on the basis of history and clinical
    signs.
A

Retrobulbar Neoplasia

-Slowly progressive
-Non painful
Mast cell tumors, orbital lymphoma are painful and rapid onset
-Unilateral exophthalmos
-Periocular swelling, exposure keratitis, retinal detachment may be present
-91% of Feline tumors are malignant and 90% of canine are malignant
-Dog average age 8yo, Cats 8-9 yo
-Survival 10 mts

Dog
-Optic nerve meningiomas
-Fibrosarcoma
-Osteosarcoma

Cats
-Malignant melanoma
-Lymphosarcoma
-Osteosarcoma
-SCC

Dx
-History
-Radiographs
-Ultrasound
-CT
-MRI
-Cytology
-FNA

Tx
-Exenteration of the orbit
-All orbit contents are excised
-Ancilliary radiation and chemotherapy

Retrobulbar Inflammation

-Cellulitis/Abscessation/Myosistis
-Acute signs
-Considerable pain
-Fever often seen
-Leukocytosis may be evident on CBC
-Tooth root abscess most common cause
-Penetration of foreign bodies through soft palate, skin or conjunctiva into orbit

Dx
-Orbital ultrasound
-Oral exam
-Dental radiograph

Tx
-Surgical drainage through oral mucosa
-Never close the tips of hemostat while instrument still in orbit as it can damage optic nerve
-Culture and sensitivity indicated
-Wound can heal by second intention
-Amoxicillin/Clavulanic acid orally

89
Q
  1. explain the pathogenesis of the enophthalmos associated with Horner’s syndrome.
A

-Loss of smooth muscle tone in the periorbita
-Due to sympathetic denervation
-Enophthalmos and protrusion of the third eyelid
-Ptosis (drooping of the upper lid)
-Relative miosis when compared to the opposite eye

90
Q

Other Inflammatory Orbital Diseases -

A

Masticatory myositis

-Exophthalmos uni or bilateral
-Pain upon opening the mouth
-Shetland sheepdogs, GSD, Golden retrievers, Weimaraners most affected
3yo most common

C/S
-Acute inflammation 10-21 days
-Eyelid edema
-Protrusion of third eyelid
-Conjunctival hyperemia

Tx
-Immunosuppressive corticosteroids
-Azathioprine may also be effective

Extraocular Polymyositis

-Immune mediated myopathy
-Females and 7-10 mts old most affected
-Bilateral mostly, not symmetrical
-Acute onset of exophthalmos
-Chemosis
-360 degrees scleral show and absence of third eyelid protrusion
-Pain not common
-Vision occasionally compromised
-Psychological stress association

Cystic Orbital Disease

-Exophthalmos
-Cysts arising from epithelial or glandular tissue
-Mucoceles can also develop
-Firm, smooth, fluctuant cysts
-Ultrasound hupoechoic and well delineated
-Tx: surgical resection curative

91
Q
  1. discuss the management of a proptosed globe and predict the visual and cosmetic prognosis based on
    initial clinical signs.
A

Proptosis of the Globe

-Traumatic displacement from the orbit TRUE EMERGENCY
-Brachycephalic breeds predisposed
-Prognosis for return to vision is guarded
-Temporary tarsorrhaphy
-Antibiotic ointment
-Systemic corticosteroids
-Sequela: strabismus, lagopththalmos, decreased tear production, corneal ulceration

92
Q
  1. identify the most common cause of strabismus likely to be encountered in a companion animal practice.
A

-Deviation of the globe from its central axis

-Common in brachycephalic breed
-Develops in response to space-occupying orbital lesions, rupture of the extra ocular muscles, and abnormalities of the CNIII, IV, VI.
-Ventrolateral deviation occurs in hydrocephalic animals with enlarged cranial cavity
-Siamese cats may appear crossed-eyed

93
Q
  1. differentiate between enucleation, exenteration and evisceration, providing one indication for each
    surgical procedure.
A

Enucleation
-Removal of the eye, eyelid margins, conjunctiva, and third eyelid
-Silicone sphere put into orbit
-Indications: neoplasia, catastrophic trauma, chronic intractable glaucoma, severe intraocular inflammation unresponsive to therapy
-Cats have short optic nerve, careful surgery or blindness in remaining eye

Exenteration
-Removal of all orbital contents
-Indicated for orbital neoplasia

Evisceration
-Removal of all intraocular contents
-Sclera incised
-Silicone sphere implanted
-Indicated for cosmetic treatment of end-stage glaucoma

Always submit tissue for histopathology

94
Q

Enophthalmos

A

Causes

-Ocular pain
-Microphthalmia
-Phthisis bulbs
-Horner’s syndrome
-Dehydration
-Loss of orbital fat
-Muscle atrophy
-Collapsed globe
-Conformational exophthalmos in dolichocephalic breeds

Tx
-Seldom indicated

95
Q

Lecture Glaucoma

A
96
Q
  1. define glaucoma.
A

-Abnormally elevated IOP incompatible with normal ocular physiology and vision
-Devastating effect on optic nerve, death of retinal ganglion cells at their axons
-Common cause of blindness in companion animals
-Primarily an inherited disorder in dogs
-Cats usually complication of chronic uveitis

97
Q
  1. discuss the normal aqueous production/outflow pathway and discuss mechanisms by which the normal
    pathway may be interrupted, resulting in glaucoma.
A

Normal IOP: 10-20 mmHg

-Decreased in outflow of aqueous humor and subsequent outflow from the eye
-Usually prior to (pupil) iridocorneal angle or within it
-Carbonic anhydrase enzyme active in secretory process of ciliary body epithelium aqueous humor production. It can be pharmacologically modified to reduce aqueous production
-Normally aqueous exits through the iridocorneal angle from the anterior chamber
-Ultimately entering the systemic circulation through the trabecular veins, sclera venous plexus, and vortex veins
-Prostaglandin analogues that increase uveoscleral outflow in the dog present a major breakthrough in glaucoma control in recent years, but not effective in the cat

98
Q
  1. identify the common clinical signs seen in acute canine glaucoma and explain the pathogenesis of those
    signs.
A

Acute Canine Glaucoma

C/S
-Subtle and highly variable
-Mild conjunctival vascular enlargement
-Increased tearing
-Variable pain
-Photophobia
Important to measure IOP on any patient with red eye
-Easy to miss signs of glaucoma

Advanced disease

-Ocular pain due to trigeminal neuralgia
-Blepharospasm
-Nicitans protrusion
-Excessive tearing
-Epsiscleral and conjunctival vessels congestion, passive process due to compromised venous outflow
-Corneal edema, pressure affects the endothelium and CN V nerve endings
-Pupillary dilation, muscular paresis due to pressure on retina/optic nerve
-Elevated IOP

Chronic

-Scleral thinning
-Decreased evidence of ocular pain
-Haab’s striae - breaks or stretch marks in Descemet’s membrane
-Iris degeneration
-Fundus lesions

99
Q
  1. define buphthalmos and explain its significance with regard to urgency of therapy and prognosis for
    vision
A
100
Q
  1. explain the importance of initiating definitive therapy as soon as possible following onset of glaucoma.
A
101
Q
  1. outline a diagnostic and medical regimen for treatment of acute glaucoma in a dog, including the
    mechanisms of drug action and prognosis for successful medical control of intraocular pressure (IOP).
A

Dx
-Tonometry
-Ophthalmology of retina, optic disc
-Gonioscopy to evaluate gross appearance of iridocorneal angle. Helps differentiate between primary and secondary glaucoma

Primary glaucoma

-No concurrent ocular disease or injury
-Breed-related, inherited
-Bilateral but one eye more affected than the other.
-Second eye affected within 8-12 mts if no treatment
-Identification of the abnormal angle substantiates need for prophylactic therapy of the second eye

Gonioscopic - Iridocorneal angle

  1. Open angle glaucoma: normal angle; Beagle
  2. Narrow angle: decreased width of angle; Crocker spaniel
  3. Pectinate ligament dysplasia (goniodysgenesis): abnormal pectinate formation, characterized by broad sheets of tissue with few flow holes; Basset hound

Secondary Glaucoma

-IOP sequela to other ocular disease or injury
-Causes: lens luxation, trauma, inflammation, neoplasia
Pupillary blockage by lens responsible for IOP increase
-Anterior uveitis produces adhesions of iris to cornea, obstructing flow through the iridocorneal angle
-Tumors invade and cause secondary inflammation, adhesions

Therapy

  1. Reverse IOP increase
    a. Medical: stabilize within 24-48 hours
    b. Surgical
    c. Combination

Drugs MOA
1. Promotes aqueous outflow (usually with miosis)
2. Dehydrate the vitreous
3. Decrease aqueous production

-Topical less potent but less side effects than systemic
-Dogs tolerate better than cats
-Remission of primary glaucoma, later additional alternate drugs
-Always aim for synergistic action
-Human drugs do not predictably work on dogs or cats

Neuroprotective agents

-Systemic calcium channel blockers (Amlodipine besylate)
-Systemic corticosteroids to combat oxygen free radicals
Prophylactic treatment of second eye is imperative
-Topical Carbonic anhydrase inhibitor (Dorzolamide or Brinzolamide) for prophylactic second eye care
-Topical Demecarium bromide solution combined with SID steroid

Refer immediately to ophthalmologist, do not wait

Primary Narrow Angle Glaucoma, Medical Tx

-2% Dorzolamide topically
-Latanoprost topically
-If no improvement: repeat Latanoprost add mannitol, recheck
-If no improvement: refer

If improved after 2% dorzolamide
-Re-evaluate in 1 hour
-Dorzolamide q8 hrs
-Latanoprost q 12 hrs
-Recheck IOP q 4-6 hors
-If stable: continue both, treat second eye prophylactically, refer for surgical evaluation

102
Q
  1. explain how the pathogenesis of glaucoma in the cat differs from that of the dog.
A

-Rarely diagnose in cats
-Signs present in dogs not present in cats
-Most common complain is increased eye size
-Cloudy eye appearance
-Increased pupil size
-Usually blind by the time of evaluation
-90% secondary glaucoma associated with chronic anterior uveitis
-Treatment defers from primary glaucoma

103
Q
  1. identify the topical drug of choice for treatment of feline glaucoma.
A
104
Q
  1. specify the normal range of intraocular pressure in the dog and cat and the target IOP required to
    prevent ongoing optic nerve damage following the onset of glaucoma.
A

Normal </= 20 mmHg