Part C: Surgery STATE

1. Diseases of the eyelids, conjunctiva and third eyelid

Conditions:

• Eyelid → entropion, ectropion, laceration, eyelid neoplasia, ectopic cilia, blepharitis, coloboma, distichiasis, trichiasis, ankyloblepharon

• conjunctival → conjunctivitis, dermoid/choristoma, chalazion, neploasia, symblepharon

• Third eyelid → prolapse/cherry eye, third eyelid flap, plasma cell infiltration, cartilage deformity, enucleation

1) Eyelid Disorders

Entropion (Inward Rolling of Eyelid Margin)

• inward rolling of edge → hair/lashes to rub directly on cornea.

• Etiology: Congenital/developmental (Shar-Pei, Chow Chow, Pug - excess skin), spastic (secondary to ocular pain/ulcers), or cicatricial (scarring). Rare in cats, but seen with chronic FHV-1/Chlamydia conjunctivitis.

• CS: Epiphora (excessive tearing), corneal ulcers, vision loss, blinking, discharge

• Medical tx: Topical antibiotics (terramycin, erythromycin), procaine penicillin, or try topical antiviral drops in cats.

• Surgical Techniques:

  • Eyelid Tacking (Puppies < 20 w): excess skin is tacked down w/vertical matress/lambert sutures (to roll the margin outward without tissue excision) then removed after a few weeks. Do not penetrate conjunctiva.

  • Hotz-Celsus Procedure (Permanent): Excision of a strip of skin of lower eyelid, then closed w/simple interrupted. Starting in the middle, and halving each segment.

  • Permanent Lateral Tarsorrhaphy: remove V-shaped segment at lateral canthus, the upper and lower lids are sutured together at that outer corner. (shortens the eyelid opening and tightens the lid so it no longer rolls inward)

  • Arrowhead Procedure: Remove arrowhead-shaped segment right next to the lateral canthus; close in a V-shape. (closing this cutout pulls the eyelid skin sideways, backward)

Ectropion (Outward Drooping of Lower Eyelid)

• Etiology: Congenital in giant/hound breeds (Bloodhound, St. Bernard, Great Dane). → affects tear drainage, leads to excessive tearing, chronic keratitis.

• Surgical Techniques:

  • Lateral Eyelid Wedge Excision: removing a full-thickness V-triangle out of the lid margin near the corner (lateral canthus), then close in 2 layers (simple continuous deep, simple interrupted skin), w/knots buried to prevent corneal irritation.

  • V-Y Plasty: Make a V-shaped incision 1 mm below the eyelid margin, excise underlying scar tissue, elevate skin flap, and close in a Y-shape.

  • Modified Kuhnt: eyelid is split like a sandwich into an outer skin layer and inner pink layer, we cut a V wedge only out of the inside layer (conjunctiva/tarsus) to tighten the structural wall. The skin on the outside is left intact, just stretched and sutured.

Laceration

• Etiology: Trauma (bite wounds, sharp objects).

• Repair ASAP to protect the cornea and preserve normal blinking. Secondary healing leads to fibrosis and corneal scarring.

• Surgical Approaches:

  • Direct Reapposition/closure (<1/3 margin loss): Align eyelid margin first using a modified figure-eight suture. Close skin with partial-thickness simple interrupted sutures.

  • Flap Reconstruction (>1/3): Advancement flaps or grafts required.

  • Temporary Tarsorrhaphy: Indicated (partial or complete closure of eyelids) if eyelid function/blinking is impaired post-op.

• Post-Op: Artificial tears + topical and systemic antibiotics.

Eyelid Neoplasia

• Most canine masses arise from Meibomian glands “oil glands lining the eyelid margins” (70–80%+ benign, e.g., sebaceous adenomas, epitheliomas). Feline masses are mostly malignant (SCC).

• Dg: History, signalment, fine needle aspiration (use eyelid plate), chest X-rays (to check for pulmonary metastasis). Treat secondary infections prior to surgery.

• Surgical removal:

  • Primary closure after excision (< 1/3 margin): remove mass. Align margin with a figure-eight suture; close skin with simple interrupted sutures.

  • H-Plasty Pedicle Advancement Flap (Lower Lid, > 1/3 margin): remove a square segment w/mass. Make triangular excisions “dog ears”. Mobilize conjunctiva, advance flap to margin. Close w/simple continuous.

  • Semi-Circular Flap (Lateral Canthus, > 1/3 margin): remove mass, make incision (2x length of removed eyelid), at lateral canthus, and excise a triangular segment at the end. Advance the skin flap. Align skin margin w/figure 8 suture. suture skin of eyelid + lateral canthus w/simple interrupted.

• Post-Op: Always submit tissue for histopathology.

• Medical Tx options include chemo, radiation, or cryotherapy.

Eyelash & Other Margin Anomalies

• Ectopic Cilia: Cilia growing from meibomian gland on the inside of eyelid (through palpebral conjunctiva) → painful, severe corneal ulceration. Tx: wedge excision of cilia with conjunctiva, electro-epilation, or cryotherapy.

• Distichiasis: Extra cilia emerging directly from Meibomian gland openings along lid margin. Tx: Cryosurgery or electro-epilation.

• Trichiasis: Normally positioned hair/cilia directed abnormally toward the cornea. Tx: Surgical excision of facial/nasal folds or lid re-alignment.

• Blepharitis: eyelid inflammation (bacterial, fungal, parasitic, or allergic).

• Hordeolum: Localized suppurative gland infection (External = Zeis/Moll glands; Internal = Meibomian gland). Tx: Warm compresses - for relief, topical antibiotics/steroids (maxitrol)

• Ankyloblepharon: eyelids does not open within 15 days post-birth. Tx: Manual separation and warm flushing.

2. Conjunctival Disorders

Condition	Etiology & Features	Surgical / Medical Treatment
Dermoid (Choristoma)	Congenital skin tumor (normal skin tissue containing hair/glands located on conjunctiva/cornea).	Superficial conjunctivectomy or keratectomy. To surgically remove mass, a temporary stay suture is set through mass, lifting mass up for easier excision.
Chalazion	Non-infectious, chronic granulomatous blockage of Meibomian/tarsal gland → Bump on eyelid.	Surgical incision and drainage.
Neoplasia of conjunctiva	Dogs: Hemangioma, limbal melanoma. Cats: Lymphosarcoma (LSA), SCC.	Localized surgical excision (benign/small under local block; large require general anesthesia).
Symblepharon	Pathological adhesion of conjunctiva to conjunctiva or cornea. Common in cats (post-FHV-1)	Surgical breakdown (indicated only if vision, drainage, or eyelid motility is impaired). can be keratectomy (surgical dissection, preventing re-adhesion → membrane graft/contact lens).

3. Third Eyelid Disorders

a) Cherry Eye (Third Eyelid Gland Prolapse)

• = when tear gland tucked inside a dog`s third eyelid pops out of place → red cherry-like mass in the inner corner of eye. Occurs when the anchor of the gland to the periorbita is weak/loose (laxity of CT). Common in Bulldogs, shi tzus.

• Pre-Op: Topical antibiotic-corticosteroid combination (if cornea is intact) to reduce inflammation.

• Treatment: Replacement, NOT excision (removal leads to Keratoconjunctivitis Sicca).

• Pocket Procedure: tucks the popped-out gland back into the pocket - by 2 conjunctival incisions on opposite sides of gland → suture opposing margins together w/simple continuous to enclose gland within a pocket → make sure to tie starting and finishing knot on the side facing away from the eye to prevent irritation.

b) Plasma Cell Infiltration (Plasmoma / Pannus of 3rd Eyelid)

• = Immune-mediated inflammation common in German Shepherds; causes depigmentation, thickening, and irregular surface of the third eyelid margin.

• Tx: Lifetime topical immunosuppression (corticosteroids, cyclosporine, or tacrolimus).

Cartilage Deformity (Everted / Inverted Cartilage)

• = the free border of 3rd eyelid rolls outwards. Common in large breeds.

• Tx: Surgical excision of the deformed/bent portion of the cartilage stem.

Third Eyelid Flap (Procedure Note/surgical technique linked)

• Indication: Temporary mechanical protective bandage for cornea after trauma like superficial non-healing/indolent ulcers or bullous keratopathy. Contraindicated in deep ulcers, descemetoceles, or corneal perforations (creates excessive pressure and blocks monitoring).

• Technique: Suture passed from dorsolateral upper eyelid conjunctiva through outer surface of third eyelid (around cartilage, avoiding posterior surface), back out upper lid, tied over a stent. Remove after 14 days.

Enucleation: the complete removal of an eyeball from the eye socket. etio: malignant tumors, severe trauma (fight), blindness, glaucoma.

NOTES:

• very briefly about the most common disorders of eyelids - wanted to know about entropion & ectropion + surgeries related to this.

• another time → only wanted to know about entropion + ectropion - defintion &CS, disorders we have in eyelashes - but did not want to talk much about it. Then asked about infectious diseases of eye (chlamydia, calici, herpes), asked alot about chlamydia + tx, what drops to use in the eyes (treat w/systemic ATB (long) + also topical ATB drops).

2. Diseases of the cornea – Keratitis, ulceration, perforation

Anatomy of the Cornea

• Corneal Layers: Epithelium → stroma → Descemet’s membrane → Endothelium.

• Limbus: Junction between the cornea and the sclera.

1. Keratitis (Non-Ulcerative Inflammation)

• = Inflammation of the cornea.

• Etiology:

  • Trauma

  • Infectious: Feline Herpesvirus-1 (FHV-1), Chlamydia (cats), Fungi.

  • Immune-Mediated: Chronic Superficial Keratitis (Pannus) — common in middle-aged German Shepherds, or surgery.

  • Eosinophilic Keratitis: cats.

• Clinical Signs: Redness, corneal opacity, blepharospasm, 3rd eyelid inflammation, white round raised spots (eosinophilic), or stromal abscessation (fungal).

• Medical Treatment: Topical antibiotics, dexpanthenol gel (lubrication), topical corticosteroids (CS) or cyclosporine (only if no ulceration is present).

• Surgical Interventions (for non-healing superficial defects):

  • Grid Keratotomy: Scratching grid lines into the stroma with a needle to promote cell adhesion/healing.

  • Diamond Burr Debridement: Mechanical burring/polishing to strip unattached epithelium and promote healing.

2. Corneal Ulceration

• Most common in brachycephalic breeds.

• Etiology:

  • Trauma & Eyelid Abnormalities: Entropion, trichiasis, ectopic cilia.

  • Ocular Surface / Systemic Disease: Dry eye (KCS), Diabetes mellitus, Cushing’s disease, Hypothyroidism.

  • Infectious: Secondary bacterial infection (Pseudomonas, Staphylococcus, Streptococcus).

  • Idiopathic: Boxer indolent ulcer (spontaneous superficial defect with non-adherent edges).

Ulcer Classification

Type	Tissue inv. + typical
Simple Superficial	Loss of corneal epithelium only; heals rapidly without scarring.
Indolent Ulcer	Superficial ulcer where epithelium fails to adhere to underlying stroma (e.g., Boxer ulcer).
Stromal Ulcer	Loss of both epithelium and varying depth of corneal stroma; heals with scar formation.
Descemetocele	Deep ulcer extending through full stroma down to Descemet’s membrane; high risk of rupture.
Melting Ulcer	Rapid enzymatic liquefaction of stroma caused by bacterial proteases/collagenases (released by Pseudomonas, b-hemolytic Strep).
Perforating Ulcer	Full-thickness rupture leading to corneal opacity (white), vascularization, and possible iris prolapse.

• Clinical Signs: Ocular pain, blepharospasm, photophobia, epiphora, discharge, corneal edema, opacity.

• Diagnostics:

  • Fluorescein Stain: Positive uptake confirms epithelial loss (adheres to open stroma; Descemet's membrane stays negative).

  • Aerobic Bacterial Culture & Sensitivity: Essential for infected or deepening stromal ulcers.

Treatment:

• Corticosteroids are strictly contraindicated as they increase matrix metalloproteinase activity (speeds up protease prod) → speeds up stromal melting.

• Medical Protocol:

  • Topical Antibiotics: Gentamicin (G+focus), Chloramphenicol (G+&-)

  • Anti-Proteases: EDTA

  • Mydriatics: Topical atropine/tropicamide

  • Systemic Analgesia: NSAIDs

  • Debridement: Manual removal of loose epithelial lips.

• Surgical Procedures (Conjunctival Flaps): make flap from bulbar conjunctiva and suture over affected area of cornea. Flap is removed after some time,. affected area will be permanently opaque.

  • Hood Graft: Indicated for small or peripheral defects. Simple interrupted sutures to suture flap over affected area, starting at the corners of flap.

  • 360-Degree Graft: Indicated for large or central severe defects. Covers the entire cornea and is sutured to itself in a horizontal mattress pattern.

3. Stromal Abscess

• = Focal accumulation of yellow-to-white inflammatory/infectious infiltrate trapped within the stromal layer.

• Medical Tx: Topical chloramphenicol, natamycin (antifungal), atropine; systemic flunixin and trimethoprim.

• Surgical Treatment: Surgical debridement combined with a pedicle conjunctival flap.

4. Corneal Perforation & Penetration

• Etiology: Trauma (scratches, bite wounds, foreign bodies), mostly seen in brachycephalic dogs, or progression of an untreated deep ulcer.

• Types:

  • Penetrating - full-thickness wound where object enters cornea but does not exit

  • Perforating - involves wound/foreign body to both enter and exit through cornea

• Clinical Signs: Severe pain, opacity, purulent discharge, eye enlargement

• Diagnostics: Seidel Test (Fluorescein stain applied to detect clear aqueous humor leakage streaming through the yellow stain).

• Treatment:

  • Immediate foreign body removal (if present),

  • intensive topical antibiotics,

  • dexpanthenol gel lubrication,

  • surgery

    • conjunctival flap if penetrating, for protection to prevent endophthalmitis (tissue covering),

    • keratoplasty/corneal grafting (transplantation of corneal tissue),

    • superficial keratectomy (excision of a part of corneal epithelium and stroma).

3. Diseases of the iris and retina

Anatomy:

Uvea: Layer of tissue under the white of the eye (sclera). Consisting of 3 parts, iris (colored part), choroid (layer of bv + CT bw. sclera + retina), and ciliary body (secreting aqueous humor - transparent fluid into the eye). - basically iris is the most anterior part of uveal tract!

Retina: Innermost, light-sensitive layer of tissue located near the optic nerve. Its function is to get focused light from the lens → convert light into neural signals → then send these to the brain for visual recognition.

A) Diseases of the Iris

1) Congenital Diseases:Congenital abnormalities of uvea - relatively frequent, but usually have little to no adverse effect on vision.

• Heterochromia: Difference in color between the two irises, or between parts of the same iris (hypopigmentation or hyperpigmentation).

• Persistent Pupillary Membrane (PPM): Failure of regression of the pupillary membrane that closes the fetal pupil. Attached to the iris at one end, with the other end potentially floating in the anterior chamber. Heritable in the Basenji.

• Anterior Uveal Cysts/Iris cysts: hollow, transilluminate.

• Polycoria (more than 1 pupillary opening within iris), aniridia (partial/no iris), coloboma (tissue defect/notch in iris/choroid, retina), dyscoria (abnormally shaped pupil),

2) Uveitis

• = Inflammation of the uveal tract/uvea (iris, ciliary body, and choroid).

  • Uveitis is anatomically classified as: Anterior, posterior, intermediate uveitis and panuveitis

  • Anterior Uveitis: Primary to the anterior segment. Includes iritis (inflammation of iris) and iridocyclitis (inflammation of both iris and ciliary body)

• Etiology: Infectious, secondary to corneal/scleral/systemic disease, idiopathic, immune-mediated, toxic, or traumatic.

  • Viral - canine hepatitis,. herpes, distemper, FeLV, FIV, FIP, rhinotracheitis. Bacterial - rickettsia, lepto & bruce. Fungi, parasite - leishmania & toxoplasma.

• Patho: Sensitized lymphocytes enter the uveal tract, participating in antibody formation or cell-mediated immunity.

• Complications: recurrence, corneal scarring, corneal endothelial degen., cataracts & secondary glaucoma

• Clinical Signs: Photophobia, blepharospasm, epiphora, discharge, impaired vision, conjunctival hyperemia, swollen iris, low intraocular pressure (IOP).

• Diagnosis: Increased schirmer tear test, reduced pupillary reflex, visual exam w/light, reduced then increased IOP. Diff. dx: conjunctivitis, glaucoma, superficial keratitis.

• Treatment: Conservative management. Includes mydriatics (atropine - to dilate pupil), cycloplegics (paralyze the smooth mm to stop spasms), anti-inflammatories (NSAIDs, steroids - Corticosteroids - prednisolone (never combine systemic steroids & systemic NSAIDs due to risk of GI ulcer!)), and antibiotics.

3) Hyphema

• = Presence of blood in the anterior chamber; serves as a strong indicator of underlying uveitis.

• Etiology: Trauma, clotting disorders, Collie eye anomaly, tumors, uveitis, glaucoma.

• Treatment: Identify underlying cause, prevent recurrent bleeding via cage rest, and control uveitis.

4) Neoplasia (uveal tumors): primary - adenocarcinoma or melanoma, sec. - lymphosarcoma. CS - swollen eye, tx - partial iridectomy or laser surgery

5) Iris atrophy: irreversible degeneration/thinning of iris→ reduced function (light reaction). Etio - inherited (cats), old age (chihuahua), secondary to glaucoma or unveitis.

B) Diseases of the Retina

1) Collie Eye Anomaly (CEA)

• = An inherited eye defect present at birth in varying degrees in rough- and smooth-coated Collies. NB - primarily a disease of chorioid (posterior uvea) → directly cause sec. retinal disease.

• Patho: Failure of full development in an area of the choroid or retina/choroid. Severely affected dogs may show abnormalities near the optic nerve entry, retinal detachment, or blood vessel ruptures (bleeding of eye). Vision is unaffected unless retinal detachment is present.

• Clinical Signs:

  • Choroid hypoplasia (a pale area of depigmentation temporal to the optic disc)

  • Colobomas of the posterior pole (missing piece/hole/pit in ocular tissue, in the back protion of eyeball - posterior segment, in/right next to optic disc)

  • Retinal detachment

  • Retinal or vitreous hemorrhage, blindness

• Diagnosis: Genetic testing (confirms disease presence or identifies carrier dogs), opthalmoscopy (hypoplasia of choroid, pale, thin areas).

Retinal Dysplasia

• = An anatomic retinal abnormality that may occur alone or alongside other ocular defects.

• Etiology: Congenital, or acquired secondary to intrauterine inflammation and retinal necrosis (e.g., canine herpesvirus). Most often in labrador/cavalier.

• Clinical Signs: Retinal folds, retinal rosettes, focal retinal degeneration, leukocoria (white pupil), microphthalmia, cataracts, nystagmus, blindness.

• Diagnosis: Ophthalmoscopic exam at 4–8 weeks of age.

Progressive Retinal Atrophy (PRA)

• = An inherited retinal photoreceptor dysplasia or degeneration leading to progressive vision loss. Affects breeds such as Setters, Cocker Spaniels, Poodles, Beagles, Dachshunds, Retrievers, etc.

• Pathogenesis: Deficiency of the enzyme cGMP phosphodiesterase causes accumulation of cGMP, which is toxic to photoreceptors. Age of onset ranges from 6 months to 12 years.

• Clinical Signs: Night blindness progressing to total blindness, slow pupillary light reflex (PLR), cataracts, tapetal fundus hyperreflexivity (reflective layer in back of eye - t.lucidum appears abnormally bright, shiny or intense when seen through an opthalmoscope).

• Diagnosis: Behavioral signs, maze testing, ophthalmoscopy, electroretinogram (ERG).

• Treatment: None.

4. Diseases of the lacrimal glands and duct. Keratitis sicca

Glands: Lacrimal gl. with lacrimal ducts (upper eyelid), tarsal gland (lower eyelid) and gland of third eyelid.

Drainage: 2 lacrimal puncta in medial canthus → 2 canaliculi → nasolacrimal duct → nasal punctum

Lacrimal apparatus = combined system for both tear production (the glands) and tear drainage (the ducts). Pathology of one will affect theother, like failure in production → surface disease (aqueous deficiency), while failure in drainage cause fluid backup and infection (like dacryocystitis).

Diseases of lacrimal gl. & duct:

A) Excretory system: drainage & outflow defects - problems here affect how tears leave the eye → cause fluid backup/local infection.

1. Dacryocystitis

• = inflammation of the lacrimal sac secondary to obstruction of the nasolacrimal sac or duct.

• CS: Epiphora (excess tearing), secondary conjunctivitis, draining fistula in lower eyelid (abnormal open tunnel, unntural discharge path where accumulated pus, fluid, drains onto face)

• Diagnosis: Head radiography with contrast media to determine the site and cause of obstruction.

• Treatment:

  • topical antibiotic (ATB) solution (fluoroquinolones ex. ofloxacin, aminoglycosites ex. gentamicin), chloramphenicol) ..

  • Temporary catheterisation using tubing or monofilament nylon suture - passed into the punctum, through duct and out through nostril, during healing. - to act as a mechanical spacer - to keep open.

  • If irreversibly damaged: Surgical creation of a new drainage pathway into the nasal cavity, nasal sinus, or mouth.

2. Imperforate Puncta

• = Congenital or acquired blockage of the lacrimal punctum, preventing tear collection → leads to overflow

  • Causes: Congenital malformation, inflammatory cells, debris, or foreign material.

• Clinical Signs: Epiphora, mucopurulent discharge, conjunctivitis.

• Diagnosis: Inability to cannulate the duct, ballooning during flushing attempts, culture, fluorescein staining.

• Treatment: Surgical incision, cannulation, and topical ATBs.

3. Obstruction of the Nasolacrimal System - tear duct

• Aetiology: Impaired tear drainage leading to overflow out of the eye. (block is further down the pipe - along, canaliculus, lacr. sac or duct)

  • Congenital: Absence of inferior canaliculus.

  • Acquired: Inflammatory causes (dacryocystitis), foreign body, or scarring (trauma/inflammation).

• Clinical Signs: Epiphora, mucopurulent discharge, conjunctivitis, pain, abscessation.

• Diagnosis: Negative fluorescein passage test, dacryocystorhinography (contrast radiography of lacrimal apparatus).

• Treatment: Flushing, topical antibiotics + corticosteroids, conjunctivorhinostomy (surgical creation of a new passage).

B) Secretory system - qualitative and quantitative tear film defects - problems here affect how tears are made or structured → eyes dries out/cornea looses its protective barrier.

1) Aqueous Deficiency - middle tear film

• Aetiology: Deficiency in lacrimal and nictitating gland components of tear production → Dry Eye.

  • Developmental: Aplasia/hypoplasia of glands (predisp. Yorkshire Terrier, Pug)

  • Acquired: Immune-mediated, Distemper, surgical removal of nictitating gland, trauma, drugs (sulfonamides), hypothyroidism etc.

  • “underlying mechanism” - that causes classic KCS..

2) Mucin Abnormality - inner tear film

• Aetiology: Evaporative dry eye associated with chronic conjunctivitis and Keratoconjunctivitis Sicca (KCS).

• Clinical Signs: Features of KCS, often without ocular discharge; normal aqueous tear production.

• Diagnosis: Clinical signs, Fluorescein Break-Up Time (FBUT), conjunctival biopsy (goblet cell quantification).

  • FBUT Values: Normal dog = ~20 seconds; Mucin deficiency = <5 seconds.

• Treatment: Topical mucomimetics, mucin replacers, topical corticosteroids (CCS).

3) Meibomian Gland Dysfunction (Lipid Deficiency) - outer tear film

• = lack of oil layer from glands → Increased evaporative tear loss, premature tear film break-up, dry eye.

  • Developmental: Eyelid defects affecting gland number and distribution.

  • Acquired: Marginal blepharitis (e.g., Staphylococcus, Streptococcus), meibomianitis.

• Pathophysiology: Secretions thicken and obstruct ducts due to glands being inflamed/blocked etc. Gland rupture leads to a diffuse granulomatous response, secondary infection, and extensive eyelid swelling.

Keratoconjunctivitis Sicca (KCS / Dry Eye)

→ Deficiency in aqueous tear production and/or mucin production (gland of the 3rd eyelid/lacrimal gland) → corneal drying and irritation (dry inflammation of cornea & conjunctiva). Mostly in cavalier, bulldogs

• Etio: Autoimmune (most common), drug-induced (atropine, sulfonamides, general anaesthetics), viral (Distemper), chronic blepharoconjunctivitis, trauma, metabolic disease (hypothyroidism), congenital, or iatrogenic (removal of prolapsed 3rd eyelid gland).

Pathogenesis

The precorneal tear film consists of three layers:

1. Outer Lipid Layer: Prevents evaporation (Meibomian glands).

2. Intermediate Aqueous Layer: Provides hydration and nutrients (Lacrimal & Nictitating glands).

3. Inner Mucin Layer: Anchors tear film to corneal epithelium (Goblet cells).

Deficiencies disrupt stability, triggering → chronic inflammation → secondary infection → corneal/conjunctival dehydration → hyperaemia → squamous metaplasia and hyperkeratinisation → corneal thickening.

Clinical Signs (Usually Bilateral)

• Acute: Keratitis, conjunctivitis, ocular pain, blepharospasm, corneal ulceration, mucoid discharge, dry appearance.

• Chronic: Mild discomfort, corneal keratinisation/pigmentation, mucoid/mucopurulent discharge, dull corneal surface.

Diagnostic Testing

• Schirmer Tear Test (STT):

  • Normal: 15–25 mm/min

  • (Note: Some references classify diagnostic cutoffs below 10 mm/min or 8 mm/min; standard clinical diagnosis begins at below 15mm/min).

• Rose Bengal Stain: Identifies dead epithelial cells - necrotic corneal/conjunctival epithelium (stains red)

Treatment Protocol:

1. Medical Management (Try Conservative Tx for at least 4 weeks first):

   • treat underlying cause, clean with NaCl or diluted betadine.

   • Lifelong cyclosporine (stimulates tear prod. + stops autoimmune destr.), preventative ATB, topical prednisolone (to decrease inflammation, CI if corneal ulcers are present).

   • methylcellulose, vit.A, hyaluronate - for hydration/lubricant

2. Surgical Options (If unresponsive to medical treatment):

   • 3rd eyelid flap - to protect cornea

   • Conjunctival Flap

   • Parotid Duct Transposition (PDT): Reroutes the parotid salivary duct to the conjunctival sac to substitute saliva for tears.

5.Glaucoma

Etiology & Pathophysiology

Glaucoma is characterized by an abnormal increase in intraocular pressure (IOP > 25–30 mmHg) resulting from obstruction of aqueous humor outflow through the trabecular meshwork at the iridocorneal angle → accumulation of aqueous humor.

• Patho:

  • Buphthalmos: Chronic elevation of IOP → global enlargement/stretching of the eye globe.

  • Corneal Changes: Stretching breaks Descemet’s membrane (producing linear corneal striae) and damages the endothelium, leading to corneal oedema.

  • Acute IOP spikes paralyze the iris sphincter and dilator muscles → fixed, dilated pupil.

  • All ocular structures are affected - pain, buphthalmia, epi-scleral congestion, mydriasis, lens luxation, ciliary body atrophy, phthisis bulbi (shruken, non-functional globe), retinal atrophy & blindness.

Classification

• Primary Glaucoma (Genetic / Breed-related; Usually Bilateral):

  • POAG (primary open-angle glaucoma) ex. Beagle

  • PNAG / PACG (primary closed/narrow-angle) ex. american cocker spaniel

  • Congenital - goniodysgenesis ex. basset hound

• Secondary Glaucoma (Consequence of existing disease; Usually Unilateral):

  • Causes: Uveitis (inflammatory cells/fibrin blocking outflow), lens luxation/subluxation, lens swelling (iris bombée), or intraocular neoplasia.

  • SOAG (secondary open angle) & SNAG (secondary narrow angle)

Clinical Presentation

Presentation	Clinical Signs
Acute	pain, red eye (episcleral congestion), depression, anorexia, diffuse corneal oedema, fixed & dilated pupil (mydriasis), acute vision loss/blindness, corneal vascularisation.
Chronic	Buphthalmos, lagophthalmos, secondary keratitis, lens luxation, corneal striae (Descemet's tears), retinal & optic nerve atrophy, eventual phthisis bulbi.

Diagnosis

1. Tonometry (IOP Measurement): Head must be held vertical, + avoid pressure on neck. IOP > 25mmHg.

2. Gonioscopy: Special lens used to visualize the iridocorneal angle (drain opening) and anterior ciliary cleft (“drain pipe underneath”, where tears drain) → to see whether entry is open (open-angle/closed) and if it is formed incorrectly (diagnose goniodysgenesis)

3. Ophthalmoscopy (Direct & Indirect)

Treatment Protocol

A. Medical Management - to decrease production or increase outflow. Depending on cause and state of angle. Prevent glaucoma in the other eye.

• Systemic drugs - reduce fluid production → acetozolamide, beta blockers (timolol, betaxolol)

• Topical

  • reduce aqueous humor - CAIs, ex. dorzolamide

  • Increase outflow - epinephrine, pilocarpine, latanoprost

Class / Route	Mechanism of Action	Examples & Considerations
Emergency Osmotic Diuretics	Rapid hyperosmotic fluid draw from the eye	Mannitol IV or Glycerol (Most effective in primary glaucoma & lens subluxation; use with caution in cardiovascular patients).
Prostaglandin Analogues (Topical)	Potent increase in uveoscleral outflow; rapid miosis (needed when goal is to rapidly pull down the intraocular pressure!)	Latanoprost. - in case of severe acute glaucoma - 1st choice. (Contraindicated in anterior lens luxation or uveitis).
Carbonic Anhydrase Inhibitors (CAIs)	Suppress aqueous humor production (for maintenance control, together with b-blocker)	Topical: Dorzolamide (Trusopt). Systemic: Methazolamide, Acetazolamide (Monitor serum potassium).
Beta-Blockers (Topical)	Decrease aqueous production (reduces ciliary blood flow)	Timolol, Betaxolol. (Use with caution in cardiac or asthmatic/pulmonary patients - lowers heart rate/function).
Miotics / Parasympathomimetics	Constrict pupil (miosis) to pull iris away from the angle and widen outflow space	Pilocarpine. (Can cause local ocular irritation and systemic side effects).
Sympathomimetics	Increase outflow facility	Epinephrine.
Analgesia	Systemic pain relief	NSAIDs or opioids as needed for intense ocular pain.

B. Surgical Management

• To Decrease Aqueous Production (Visual or Non-Visual Eyes):

  • Targets: partial or complete destruction of ciliary body

  • Cyclocryotherapy: Destruction of ciliary body epithelium (freezing probes) or Cyclophotocoagulation (using YAG laser = burns the ciliary body to stop production - NB! i notata det sto at det her increase outflow ??? men gir ikje heilt mening det??)

• To Increase Outflow (Visual Eyes):

  • targets drainage path

  • Gonioimplants / shunts - passively drain aqueous humor to the subconjunctival space

  • Lens extraction - remove blockage

  • iridectomy (create bypass)

• End-Stage / Non-Visual Painful Eyes:

  • Enucleation or Evisceration with Intraocular Prosthesis.

6.Diseases of the lens. Neoplasia of the eye

Diseases of the Lens

1. Cataract→ An opacity of the lens or its capsule resulting from structural changes in lens fibres or proteins (breaks down, clumps together).

Classification:

• By Location: Anterior capsular, anterior subcapsular, cortical, equatorial, nuclear, posterior subcapsular, posterior capsular.

• By Age of Onset: Congenital, developmental, juvenile, senile.

• By Etiology:

  • Primary: Inherited.

  • Secondary: Uveitis, trauma, infection, diabetes mellitus, radiation, toxic, nutritional deficiency, senility.

• By Consistency: Fluid, soft, hard.

Classification acc. to Stage of Development

Stage	Pathological Characteristics	Vision Status
Incipient	Early, focal opacity.	Sight unaffected.
Immature	Extensive opacity involving most of the lens; tapetal reflection still partially visible.	Vision impaired, but animal still has sight.
Mature	Complete lens opacity; no tapetal reflection visible on ophthalmoscopy.	Complete blindness in affected eye.
Hypermature	Proteolysis causes lens liquefaction and resorption; capsule appears wrinkled; anterior chamber deepens.	Blind; high risk of secondary phacolytic uveitis.

Clinical Signs

• Increased lens opacity and altered lens volume.

• Visual impairment progressing to complete blindness. Non-painful in itself.

Diagnosis: Opthalmological exam (opaque lens, increased size)

Treatment

• Medical Management:

  • Mydriatics (Atropine, Tropicamide): Dilate pupils in early stages to permit vision around focal opacities.

  • Aldose Reductase Inhibitors: Slow progression in diabetic cataracts.

  • Antioxidants (Topical/Systemic): Vitamin E, zinc ascorbate, carnosine.

• Surgery (Definitive Treatment):

  • Prerequisites: Functional retina, controlled ocular inflammation (pre-op topical steroids/NSAIDs), absence of active co-existing ocular disease, patient/client compliance.

  • Extracapsular Cataract Extraction (ECCE): Removal of the lens while leaving the capsule.

  • Intracapsular Cataract Extraction (ICCE): Complete removal of the entire lens along with its capsule.

  • Phacofragmentation: Ultrasonic disruption and irrigation/aspiration of the lens nucleus through a micro-incision.

2. Lens-Induced Uveitis (LIU)

→ Inflammation of uvea triggered by the exposure of lens proteins (Ag`s) to the aqueous humor. Hypersensitivity type IV reaction (Ag + Ab → AgAb complex → uveitis).

• Phacolytic Uveitis: Degradation of lens proteins (cataract) - in hypermature cataracts (lens capsule cannot hold onto proteins) → leakage → humoral & cell-mediated immune response. Mostly a mild, self-limiting if managed. Common in older dogs. Tx: topical anti-inflammatory agents (CCS, NSAIDs), surgery not typical.

• Phacoclastic Uveitis: Traumatic rupture of lens capsule → exposes massive amounts of intact lens Ag to aqueous humor (class II MHC T-cells + MF → severe cell-mediated immune reaction). Rapidly progressive, destructive inflammation. Tx (google): surgical removal of damaged lens + anti-inflammatory therapy.

• Tx general for LIU → Topical anti-inflammatory agents (corticosteroids - 1st line), NSAIDs

3. Lens Luxation

→ Displacement of the lens from the hyaloid fossa due to tearing of the ciliary zonules. (lens zonules = tiny thread-like fibers holding the lens of eye firmly in place/suspensory ligaments).

Etiology/classification:

• Primary (Hereditary): Inherent weakness/abnormal insertion of lens zonules, leading to rupture early in life (<5yrs). predisp. in terrier breeds, miniature schnauzers.

• Secondary (Acquired) to: blunt trauma, chronic glaucoma (buphthalmos stretching zonules), uveitis, tumors, cataracts

Clinical Manifestation by Position

• Subluxation: Partial zonular rupture. Presentation includes an aphakic crescent (half-moon edge of lens in pupil), instability of iris and lens.

• Anterior Luxation: Lens displaces into the anterior chamber. Presents as an acute emergency: glaucoma, corneal edema.

• Posterior Luxation: Lens drops into the vitreous cavity. May be clinically silent or induce ocular inflammation / glaucoma.

Diagnostic Findings: Iridodonesis (iris vibration), lens movement, vitreous strands/fibers floating throught he pupil into anterior chamber - Opthalmological exam.

CS: Pain, whitening of eye, squinting, epiphora (excessive tearing), edema, glaucoma, uveitis.

Treatment Protocol

1. Medical Stabilization: Reduce IOP using hyperosmotics (Mannitol IV) or carbonic anhydrase inhibitors; manage secondary anterior uveitis with topical anti-inflammatories. (Note: Avoid miotics like Pilocarpine in anterior luxation as they trap the lens in the anterior chamber).

2. Surgical Extraction: for anterior luxation lens - in visual or potentially visual eyes via intracapsular extraction (ICCE) or phacoemulsification (w/USG energy).

3. Enucleation: Indicated if the eye is permanently blind, hyper-pressurized of unmanaged high IOP, and painful.

Neoplasia of the Eye

Tx: radiation, Laser ablation, cryosurgery, chemotherapy, enucleation depending..

1) Intraocular & Uveal Neoplasia

• Iris Melanoma / Anterior Uveal Melanoma:

  • Most common primary intraocular tumor in dogs.

  • Manifests as dark hyperpigmentation of the iris, progressive mass growth, dyscoria (abnormal pupil shape), and secondary glaucoma due to angle occlusion.

  • Metastatic Potential: Slow-growing; potential to metastasize to lungs, liver, and spleen.

  • Treatment: Diode laser photocoagulation (for small/localized lesions) or enucleation.

• Ciliary Body Neoplasia (Adenoma / Adenocarcinoma):

  • Arises behind the iris.

  • Manifests as a pink/red mass visible through the pupil, secondary retinal detachment → secondary glaucoma. swollen conjunctiva/prominent 3rd eyelid, mydriasis.

  • Treatment: Surgical excision or enucleation.

• Uveal Lymphoma (Lymphosarcoma):

  • Secondary metastatic manifestation of systemic lymphoma. Bilateral pinkish-white infiltrates/mass in the anterior uvea, anterior uveitis, hyphaema, and secondary glaucoma.

  • Treatment: Systemic chemotherapy.

2. Other:

• Eyelid Neoplasia:

  • Dogs: Predominantly benign (Meibomian/Sebaceous gland adenoma, papilloma, melanoma).

  • Cats: Predominantly malignant (Squamous cell carcinoma [SCC], especially in white-pigmented eyelids).

  • Treatment: surgical resection, creyo, chemo, laser ablation.

• Conjunctival & Corneal Neoplasia:

  • Conjunctival: Commonly malignant (SCC, hemangiosarcoma, melanoma).

  • Corneal: Rare; primary malignant melanoma.

• Orbital Neoplasia: Almost exclusively malignant (Osteosarcoma, Fibrosarcoma, Adenosarcoma).

(Quick Reference)

                            [ Main points  ]
                                     │
      ┌──────────────────────────────┼──────────────────────────────┐
      ▼                              ▼                              ▼
 [ CATARACT SURGERY ]       [ LENS LUXATION ]              [ NEOPLASIA ]
 ├─ Extracapsular (ECCE)    ├─ Anterior (Emergency!        ├─ Eyelid (Dog=Benign,
 ├─ Intracapsular (ICCE)    │   Glaucoma + Edema)          │   Cat=SCC/Malignant)
 └─ Phacoemulsification     └─ Posterior (Vitreous/Silent)  └─ Orb

NOTES:

• just started with different classifications of cataract, then they just asked about treatment. Only wanted the names of different procedures (ex. phacofragmentation, intra and extracapsular extraction). Nothing on etiology or complications.

• For lens lux - only said difference between posterior and anterior before they cut me off

• Neoplasia - just listed what structures are most prone, types of tumor, usual treatment (ex. cryo).

7. Proptosis of the eyeball. Blindness.

1) Proptosis = Protrusion of the eyeball (anterior displacement of eyeball from orbit). Exophthalmus means the same thing, and this term is usually used when describing proptosis.

Aetiology

• Congenital (Rare): mucocele (cyst of salivary gland). Brachycephalic breeds. Arteriovenous fistula.

• Acquired: TRAUMA (primary cause), abscess, neoplasia, Orbital hemorrhage and swelling, acute eosinophilic myositis, periorbital cellulitis (foreign body, infection), vascular disorders.

Pathogenesis

• Traumatic proptosis may follow blunt trauma (e.g., being hit by a car, fight with another animal) → during trauma, the globe is luxated from the orbit, and eyelid spasms prevent its retraction → secondary orbital hemorrhage and swelling displace the globe further from the orbit.

• Complications: Corneal ulceration, enophthalmia, optic nerve degeneration, keratoconjunctivitis sicca, and medial rectus muscle injury.

Clinical Signs

• Exophthalmos (protrusion of the globe from the orbit).

• Fever, reddened discoloured swelling posterior to last upper molar, pain on jaw manipulation.

Treatment

• Conservative: Systemic antibiotics, moistening of eye.

• Surgical: Replace eye — lateral canthotomy and complete temporary tarsorrhaphy (for 2w). with usually two or three interrupted horizontal mattress sutures (use sutures on the skin and eyelid margins, be careful to not penetrate the conjunctiva).

                    [ CLIENT CALL / INITIAL ADVICE ]
                                   │
               Keep eye MOIST (Sterile Saline / Lube)
               DO NOT touch or rub ──► IMMED. CLINIC VISIT
                                   │
                                   ▼
                       [ CLINICAL EVALUATION ]
                                   │
         ┌─────────────────────────┴─────────────────────────┐
         ▼                                                   ▼
[ GLOBE SAVABLE? ]                                  [ GLOBE UNSAVABLE? ]
├─ Direct/Consensual PLR present                   ├─ >2 Extraocular muscles torn
├─ Intact globe & cornea                           ├─ Complete optic nerve avulsion
└─ Intraocular structures intact                   ├─ Ruptured globe / Hyphema
         │                                         └─ Severe posterior segment damage
         ▼                                                   ▼
   REPOSITION SURGERY                                   ENUCLEATION
PLR = pupillary light reflex test. 

2) BLINDNESS= state of being totally sightless in both eyes. Blindness can be temporary or permanent, complete or partial.

Visual deficits may result from lesions at any level of the central visual pathways from the optic nerve to the occipital lobe of the cerebral cortex (optic nerves, optic chiasma, optic tracts, and optic radiation).

Causes

• Disease affecting structure of the eye: Cornea, anterior/posterior chambers, iris, lens, retina, or optic disc.

• Disease affecting neurological pathway and CNS: Cranial nerves and CNS.

Diagnosis

• Evaluation includes thorough ophthalmic and general physical examinations + neuro exam because many systemic diseases may cause blindness.

• Subjective/Visual Tests: Menace test, dazzle reflex, maze test in both light and dark illumination, electroretinography, and visual evoked potentials.

• Other: Cerebrospinal fluid analysis (culture, serology, cytology), CT, MRI, US, and X-ray, blood test.

Types of Vision Loss

• Central/cortical blindness: total or partial loss of vision caused by damage to the brain`s occipital cortex.

  • Can be acquired, congenital or transient. Typical: ischemic stroke, cardiac surgery, encephalitis, meningitis.

• Acute vision loss: sudden onset of vision loss, bilateral loss is more common. Caused by trauma, glaucoma, intraocular hemorrhages, retinal detachment.

• Progressive vision loss: slow, developing loss of vision by chronic lesions - glaucoma, keratitis, uveitis, cataract etc.

• Congenital vision loss: present from birth due to structural developmental defects/inherited issues - gross ocular malformation (anophthalmos/microphthalmos), collie eye anomaly, retinal dysplasia.

NOTE:

• The queen of eyes wanted to know → what is proptosis, main cause (trauma), if client called you and said “my babys eye is hanging out what do i do” → you say keep it moist and come to the clinic ASAP. After you need to decide if you enucleate or put it back in and if you put it back in how to do it → put it in and suture it in place, monitor for next 2weeks.

• For blindness, all she wanted to know was about glaucoma, and problems with the retina that can cause blindness.

8. Evaluation and therapeutic surgical methods for eye diseases, diagnosis and therapy.

PHYSICAL EXAMINATION

• Clinical Signs: Discharge (mucous = irritation, green = infection), red irritated eye, cloudiness, difference in pupil size, aversion to light, squinting, exophthalmos.

• Observation: Should assess symmetry, conformation, and gross lesions.

• Palpation: around eye and head, exclude skin and dental problems as the origin of eye issue.

OPHTHALMIC EXAMINATION

A standard ophthalmic exam is a comprehensive series of tests that checks vision and the health of the animal's eyes. When examining the eye, a dark room with red light is recommended.

a) Behavioural and Vision Examination

Tests the animal's ability to navigate and orientate itself.

• Tracking: Drop cotton ball and check if dog follows.

• Maze Test: Placement of obstacles around the room and assess the dog's ability to navigate around the objects (in darkness and light), stairways.

• Placing - see if they place their feet on a surface when they can see it

b) Neuro-ophthalmic and Vision Tests

The neuro-ophthalmic examination is a tool that localizes a defect to the nervous system or the eye.

• Pupillary Light Reflex (PLR): Shine a bright light into the lateral aspect of each eye and evaluate the pupil constriction.

  • Tests: Cranial nerve II and III (Nervus opticus and N. oculomotorius).

• Menace Response: Make a threatening movement towards the eye. A normal response is to blink with aversion of head.

  • Tests: Cranial nerve II (optic), III (oculomotor), VI (abducens), VII (facialis).

• Dazzle Reflex: Shine a strong light into each eye in turn. Normal is to blink/avoid.

• Palpebral Reflex: Touch of medial and lateral canthus usually initiates a normal blink response.

  • Tests: Cranial nerve V, VI, VII.

c) Tear Film Products tests (quantitative)

The nasolacrimal system and preocular tear film are evaluated by considering both the secretory and excretory components.

• Schirmer Tear Test: Measure aqueous layer of tear film for 60 seconds.

  • Normal: >15mm/min, while <8-10 indicates the risk of Keratoconjunctivitis sicca (dry eye syndrome)

• Phenol Red Thread Test: New, fast, and equally accurate method. Only 15 sec is needed, and the test is recommended for small mammals.

  • Normal range in cats: normal is 18.4 - 27.7 mm/15sec.

d) Fluorescein Test (qualitative / structural)

• Fluorescein test - for looking at corneal ulcers - we apply flurescein dye to evaluate corneal surface, film or nasolacrimal drainage.

• Outer layer of eye (Epithelium) = oil-based (lipid-selective), water-based fluids like fluorescein dye cannot soak into it. BUT if layer is scratched/torn/ulcerated → inner layer exposed (stroma) acts like a sponge, absorbing the green dye. Green spot = ulcer/eroison! NOTE: Drops increase risk of pseudomonas infections, thus we use strips instead!

• Corneal staining - stain areas of epithelium, where it may not be intact

• Tear Breakup Time: Quality of tear film. How long will fluorescein drop stay on eye surface.

  • Normal: 20sec.

• Jones Test: Test passage of nasolacrimal duct. Drop on cornea, stain nose/mouth. If negative — try to flush. (fluroscein stain).

e) Rose Bengal Test

• to look at corneal & conjunctival epithelium - health.

• RED COLOR → Stains dead cells → defect in mucin layer of tear film

• ex. herpesvirus in cats (rose bengal is retained by cornea & conjunctiva in keratitis).

f) Intraocular Pressure (IOP)

• Normal: 15-25 mm/Hg (low = uveitis, high = glaucoma)

• Asess IOP first during an examination as any further handling of animal can cause an increase!

  • Tonovet - probe touches cornea 5x. (best option), Tonopen

  • Old other apparatus - schiøtz. Not for cat

  • Reptropulsion - can feel hardness of eyelobe w/fingers too. (Avoid pressing of jugular as this will increase pressure).

g) Ophthalmoscope

1. Direct Ophthalmoscope: Fundus, anterior eye, has filters, good magnification.

2. Indirect Ophthalmoscope: Less magnification, upside down image.

3. Fundus Camera: iPhone with lens.

4. Optical Coherence Tomography (OCT): All layers of retina and cornea, also angle.

h) Gonioscope

Gonioscopy involves examination of the drainage angle with a special lens (goniolens) and is separate from routine eye examination. The technique is used to detect goniodysgenesis (defective development of the drainage angle); an abnormality of the eye which predisposes to primary angle closure/closed angle glaucoma.

i) Ultrasound

For examination of lens luxation, detachment of retina, retrobulbar problems, and nervous problems. Eyedrops, gel on probe, directly on eye or eyelid.

j) Electroretinography (ERG)

Electrodes on retinal surface — response of retina, amplitude of waves.

k) Corneal Pachymetry

Measure thickness of cornea. Only for scientific research.

SURGICAL TREATMENTS OF EYE AND EYELID

• Eyelid Laceration Repair: Figure-of-8 suture (margin) and simple interrupted.

• Temporary Tacking Suture: Lembert (vertical mattress — far near near far). Tacking is the removal of inversion of eyelid by temporary mattress suture.

• Permanent Tacking Suture: Hotz-Celsus procedure for entropion.

• Y-U Entropion Repair: Removal of semilunar piece of skin on eyelid to permanently correct inversion.

• Modified Kuhnt.

• Excision of Eyelid: Removal of tumor, V-shape excision, figure-of-8 suture on margin.

• Eyelobe Removal (Enucleation):

  • Transpalpebral: Incision around eyelid margin, suture margins together, cut tissue of orbit, place hemostat on artery.

  • Transconjunctival: Removal of only eyeball. Note: Remove 3rd eyelid and margin of eyelid.

GENERAL TREATMENT

• Antibiotics: Gentamicin and neomycin (G+), cephalexin and chloramphenicol (G-).

• Anti-fungals: Itraconazole.

• NSAIDs: Flunixin.

• Corticosteroids: Dexamethasone, prednisolone (not if broken epithelium).

• Parasympathomimetics: Carbachol, pilocarpine.

• ACE-inhibitors: Demecarium, neostigmine.

• Others: Glaucoma (carbonic anhydrase inhibitors, beta blockers, diuretics, mannitol).