Ocular Emergencies
World Small Animal Veterinary Association Congress Proceedings, 2019

F. Ollivier

Clinique vétérinaire d’ophtalmologie Ophtalmo Vétérinaire, Inc., Montréal, QC, Canada


When do we have to face an ocular emergency?

  • Ocular pain
  • Abnormality of globe position
  • Sudden blindness
  • Change of eye appearance


  • Abnormal position of the globe(s)
  • Eyelid laceration
  • Corneal injuries
  • Glaucoma
  • Uveitis
  • Sudden blindness

Abnormal Position of the Globe(s)

  • Three types
    • Exophthalmia
      • Cellulitis/abscess
      • Myositis (eosinophilic m./extra-ocular m.)
      • Neoplasia (primary/secondary)
      • Trauma of the orbit (hematoma/fracture)
    • Enophthalmia
      • Ocular pain (ulcer/uveitis…)
      • Horner’s syndrome
    • Proptosis
      • Trauma
      • Predisposed breeds (brachycephalic)
  • Clinical signs
    • Exophthalmia
    • NM protrusion
    • Swelling (chemosis)
    • Strabismus
  • Workup
    • PE
    • Ocular examination
    • Retropulsion
    • Exploration of the mouth
    • Imaging
    • U/S
    • X-ray
  • Therapeutic approach
    • Temporary until determination of the cause
    • Pain management
    • Globe protection (lubrication, tarsorrhaphy)


  • Clinical signs
    • Proptosis = eyelid behind the equator of the globe
    • Swelling (chemosis)
    • Strabismus
    • Corneal lesions
    • Intraocular lesions
  • Assessment and prognostic
    • PLR (fixed dilated/miosis)
    • Globe integrity
    • Corneal integrity
    • Extraocular muscles
    • Intraocular lesions
  • Therapeutic approach
    • Main goal: save the eyeball
    • Pain management
    • Keep cornea moistened/lubricated
    • General anesthesia
      • Lateral canthotomy (±)
      • Prep the eye (diluted betadine 1:50)
      • Globe replacement
      • Tarsorrhaphy (4/0–5/0, stents)
    • E-collar
    • Medical treatment: systemic AID, topical AB

Eyelid Laceration

  • Clinical signs: Easy….
  • Basics
    • Check orbital bones/head integrity and globe integrity
    • Restore eyelid integrity and function
    • Surgical repair ASAP (ideally <4 h)
    • Minimal trimming of the wound margins
    • Apposition of the eyelid margin first
    • SI suture (silk 4/0–5/0)
    • E-collar
  • Medical treatment: sys AID, sys AB, topical AB

Corneal Injuries

Corneal Ulcers

Making the diagnosis of a corneal ulcer is critical for the welfare of the patient. It is the difference between sight and blindness, or a small scar and a large scar. Assume ulcers will get worse! Treat aggressively.

Normal healing: Corneal epithelium is a barrier against bacteria and fungus. In simple traumatic corneal injuries in which a small amount of epithelium is removed, healing is rapid (5–7 days) (about 0.5–1 mm/day).

In cases of noninfected, mid-stromal ulcers, healing is about 0.6 mm/day with a pronounced fibrovascular healing response.

If the ulcer becomes infected or the epithelium is unable to attach to the stroma, healing is delayed, and progression to a deep stromal ulcer may occur. Proteinases, mainly matrix metalloproteinases (MMP), are produced by keratocytes, tear film PMNs and microbes. In infected ulcers, proteinases may digest stromal collagen to cause a descemetocele and iris prolapse (within 24 h). Corneal degeneration due to proteases is referred to as “melting.” Ulcers in which proteases are active have a grayish, gelatinous appearance which must be distinguished from corneal edema. The action of proteases is potentiated by topical [sic].

Abnormal healing: Uncomplicated corneal ulcers will heal within 5 to 7 days, unless:

  • The cause is still present
  • It is infected
  • It has a basement membrane defect (indolent)
  • Topical corticosteroids are used (retard epithelialization, activate collagenase, and decrease stromal wound strength)

Classification of Corneal Ulcers

  • Depth
    • Superficial
    • Deep
    • Descemetocele
    • Perforation
  • Causes
    • Keratoconjunctivitis sicca (KCS)
    • Lid abnormalities
    • Ciliary disorders
    • Physical irritants
    • Infectious agent: herpes virus, bacteria, fungus
    • Neurotrophic (lack of sensation of ophthalmic branch of CN 5)
    • Neuroparalytic (CN 7 paralysis)
    • Foreign bodies behind third eyelid
    • Trauma
  • Speed of progression
    • Melting
    • Indolent

Clinical signs

  • Blepharospasm
  • Photophobia
  • Epiphora
  • Eyelid swelling
  • Conjunctival swelling
  • Signs of anterior uveitis-associated: miosis, fibrin, hypopyon
  • Corneal edema
  • Rough depressed area
  • Missing outer layer of cornea


  • Evaluation at distance (discharge, symmetry)
  • Menace
  • Dazzle
  • Blinking
  • Pupil size
  • PLRs
  • Slit lamp examination
  • Schirmer tear test
  • Corneal culture
  • Fluorescein stain
    • Detects a corneal epithelial, stromal ulcer—stains stroma, not epithelium
    • Seidel test
    • All red, inflamed, or painful eyes should be routinely stained with fluorescein
  • Rose bengal
    • Poor stability of the PTF and inadequate protection of the corneal epithelium
    • Very small superficial ulcers and erosions
  • Corneal scraping for cytology
  • Look for an underlying cause (KCS, distichia, trichiasis, entropion)


  • Questions to ask yourself
    • Infected?
    • Depth?
    • Melting?
    • Uveitis-associated?
  • Medical treatment
    • Determine and eliminate etiology (e.g., KCS, entropion, infection)
    • Prevent or treat infection (broad-spectrum topical antibiotics, culture and sensitivity tests)
    • Prevent progression (melting)
    • Treat uveitis
      • Topical atropine: cycloplegia/mydriasis
      • Topical NSAIDs (careful)
      • No steroids
    • Prevent self-trauma: E-collar
    • Ulcers can degenerate even if sterile!
    • Antibiotics
      • Basics: Topical application q 2 hr to q 8 h of broad-spectrum antibiotic (neomycin-polymyxin-gramicidin) if not melting and before culture results
      • If melting ulcer:
        • Suspect Pseudomonas (gentamycin, tobramycin, ciprofloxacin, amikacin)
        • Suspect β-hemolytic Streptococcus (chloramphenicol, cefazolin, bacitracin)
    • Collagenolysis (melting) prevention
      • Serum (α2 macroglobulin and α1 proteinase inhibitor) (q 1 h)
      • 5–10% N-acetylcysteine (NAC)
      • 0.05–0.2% EDTA
      • Galardin (MMP inhibitor)
      • Doxycycline (topical 0.1% or sys)
    • Uveitis treatment
      • Atropine: BID or SID initially (depends if degree of uveitis)
        • Mydriatic, cycloplegic, and decrease vessel leakage
        • Careful with KCS induced by atropine
      • Systemic anti-inflammatory: NSAIDs—Rimadyl or meloxicam (depends on the degree of uveitis)
      • Topical anti-inflammatory: flurbiprofen, diclofenac (BID to TID)
        • Careful—may get keratomalacia
      • Corticosteroids are contraindicated in case of corneal ulcers
  • Surgical treatment
    • Debridement, keratectomy, keratotomy: to remove necrotic tissue and bacterial debris, remove hyaline membrane, superficial punctate or grid keratotomy with a 20 G needle
      • Indications: necrosis, melting, indolent ulcers
    • Conjunctival graft: pedicle conjunctival graft
    • Biomaterials: submucosa or porcine intestine or porcine bladder (BIOSISTs, ACELL), amniotic membrane
    • Indications: large and/or deep ulcers, descemetoceles, perforated ulcers
    • PK: deep corneal ulcers, descemetoceles, endothelial dystrophy

Guide for the Treatment of Corneal Ulcers

  • Superficial ulcer: Broad-spectrum AB, ± atropine, E-collar
  • Superficial ulcer in cats: Broad-spectrum AB (tetracycline), ± atropine, anti-viral, L-lysine PO, E-collar
  • Non-healing ulcer: Broad-spectrum AB, ± atropine, E-collar, serum, Muro 128
    • If does not heal: debridement, scraping, grid keratotomy
  • Stromal ulcer: Broad-spectrum AB, atropine, sys NSAIDs, anti-collagenases, E-collar
    • If <50% stromal depth, medical management is appropriate for initial management
    • If ≥50% stromal depth or progressive depth or area despite medical management, consider surgery (keratectomy + conjunctival pedicle flap, corneal graft)
  • Melting corneal ulcer: Ulcers infected or treated with steroids
    • Very aggressive medical and/or surgical therapy
    • AB initially q 1–2 h
    • Antifungal q 2–4 h if + for hyphae
    • Atropine q 12 h until dilated
    • Serum and EDTA q 1 h
    • Sys doxy (5 mg/kg PO BID or 10 mg/kg PO SID)
    • Sys NSAIDs
    • (Keratectomy and conjunctival flap)
  • Monitoring: Eyes with ulcers should show reduced fluorescein uptake and the eye be less painful in 24–48 hours. If not, consider that a resistant bacterial strain or a fungus could be present, or other complicating factors. Melting ulcers should show an increase in stromal rigidity in the first 24 hours. If not, surgery is indicated as corneal rupture is possible
  • Descemetocele: Ulcer through entire stroma leaving only Descemet’s membrane and endothelium
    • Prior to referral: Broad-spectrum AB, atropine, sys NSAIDs, sys AB, ± anti-collagenases, E-collar
    • Surgical intervention—referral
      • If very small: glue, primary sutures
      • If larger: surgery (conjunctival pedicle flap, corneal graft)
  • Perforated corneal ulcer:
    • Prior to referral: Topical AB drops (not ointments), systemic AB and NSAIDs, E-collar for trip
    • Surgical intervention—referral
      • Reduce iris prolapse if present
      • Synthetic or frozen corneal graft w/conjunctival graft
      • Primary suturing if <1 mm in diameter ± conj graft

Corneal Foreign Bodies

  • Remove with irrigation, needle, forceps
  • Treat with antibiotics and atropine
  • Always examine entire eye


  • Aqueous humor dynamics and intraocular pressure
    • Balance between production and drainage keeps intraocular pressure (IOP) within normal range (15–25 mm Hg)
    • IOP varies with time of the day, age, position, blepharospasm, drugs (i.e., anesthetics, caffeine, steroids)
  • Glaucoma = increased IOP with associated visual defects (over 25 mm Hg in dogs and 31 mm Hg in cats)
    • IOP increase most commonly due to increased resistance to outflow
  • Glaucoma types
    • Over 42 breeds of dogs affected; up to 5.5% of the dog population affected
    • Two main types: primary glaucoma (30%) and secondary glaucoma (70%)
      • Primary glaucomas: two types
        • Angle open (10%) and narrow/closed (90%)
        • Bilateral glaucomas in predisposed breeds
          • Goniodysgenesis (pectinate ligament dysplasia)
            • Breeds: Bouvier des Flandres, Great Dane, Siberian husky
      • Secondary glaucomas
          • Have a detectable cause
          • Most frequent types include:
            • Cataract formation and lens-induced uveitis
            • Lens displacement
            • Intraocular tumors
            • Intraocular inflammation

Clinical Signs

  • Acute changes:
    • Vary with level of IOP (signs when IOP above 40 mm Hg)
    • Mydriasis
    • Corneal edema
    • Congested episcleral vessels
    • Blepharospasm (ocular pain)
    • Vision loss or blindness
    • ± Aqueous flare
  • Chronic changes:
    • Buphthalmia
    • Visual deficits
    • Corneal striae (Haab’s striae) and other keratopathies
    • Lens subluxation/luxation
    • Excavation/cupping optic nerve head
      • Optic nerve “cupping” is due to ON axonal loss, and rotation, compression and posterior bowing of the lamina cribrosa
      • Cupping is unique to glaucoma
    • Retinal degeneration


  • Diagnosis tool = tonometer
  • Normal canine and feline IOP: 15 to 25 mm Hg
  • Compare both eyes
    • Generally, difference in IOP between fellow eyes <5–8 mm Hg
  • Digital tonometry: crude IOP evaluation, but unsatisfactory for monitoring
  • Schiotz indentation tonometer
  • Tono-Pen applanation tonometer
  • Tonovet rebound tonometer


  • Presently no cure for glaucoma
  • Objectives of therapy

a.  Maintain vision and eliminate pain by lowering the IOP by increasing aqueous outflow, decreasing aqueous production

b.  Prevent or delay glaucoma in the other eye

Treatment of Acute Glaucoma

  • Need to rapidly decrease IOP
  • Topical prostaglandin—latanoprost or others (not if lens luxation) increases uveoscleral outflow
  • Hyperosmotic agents—dehydrate vitreous, reduce ultrafiltration, 20% mannitol or 50% glycerol
  • Anterior chamber paracentesis removes aqueous through peripheral cornea

Maintenance of Medical Therapy

  • Drugs to decrease aqueous production
    • Systemic carbonic anhydrase inhibitors (CAIs)
      • Side effects: metabolic acidosis, anorexia, depression (especially cats!)
    • Topical CAIs—same effect as systemic
    • Safer β-adrenergic antagonists (topical)
      • Reduce formation aqueous humor, no effect on outflow
      • Side effects: bradycardia, especially in small dogs
  • Drugs to increase outflow
    • Prostaglandin analogs (topical)
    • Parasympathomimetics (topical)
  • Additional drugs
    • Calcium channel blockers
    • Glutamate inhibitors
    • Systemic corticosteroids (in selected cases)
  • Prophylactic treatment
    • Essentially all types of primary glaucomas are bilateral!
    • Need to treat fellow normotensive eye with:
      • Topical beta-blocker (0.5% timolol maleate BID)
      • Topical CAI (2% Trusopt BID/TID)

Medical vs. Surgical Treatment

The iridocorneal angle gradually closes in most types of glaucoma and the initially effective treatment becomes inadequate. Surgery is the option available when vision continues to diminish and IOP continues to increase in spite of maximum medical therapy.

Surgical Therapy

  • Visual eyes
    • Cyclodestructive procedures (decrease aqueous production)
      • Lasers (cyclophotoablation) or cryocycloablation (cyclocryoablation)
    • Fistulization procedures (increase outflow)
      • Gonio shunts
  • Blind eyes
    • Ciliary body ablation
    • Intraocular prosthesis
    • Enucleation—removes source of pain

Feline Glaucoma

  • POAG in Siamese and Burmese
  • Secondary glaucomas from uveitis and tumors are most common
  • Clinical signs can be very discreet (often only anisocoria/mydriasis, buphthalmia)
  • Latanoprost (Xalatan) not effective in cats



  • Idiopathic
  • Infection (TBD, FIV, FIV, FeLV, herpes, toxo, crypto)
  • Immune-mediated (VKH, LIU)
  • Neoplasia
  • Trauma
  • Secondary to another ocular condition (ulcer, cataract, lens capsule rupture)

Clinical signs

  • Photophobia
  • Epiphora
  • Prolapsed nictitans
  • Conjunctivitis
  • Scleral injection
  • Corneal edema
  • KP
  • Aqueous flare
  • Hyphema and/or hypopyon
  • Miosis
  • Hypotony
  • Glaucoma may result


  • Etiologic
  • Mydriatic/cycloplegic: atropine
  • Topical ± systemic AID

Sudden Blindness

  • Workup
    • Visual assessment
    • PE
    • Ocular examination
      • Blindness due to ocular condition (RD, optic neuritis, SARDS)
      • Central blindness
  • SARDS: Sudden acquired retinal degeneration
    • Non-inflammatory degeneration and loss of photoreceptors, female, obese, 8–10 y, cushingoid…
  • Treatment if blindness due to ocular condition:
    • Important to know if it is degenerative (SARDS) or inflammatory (RD, neuritis)
  • Treatment if blindness due to systemic disease:
    • Infectious, inflammatory, systemic hypertension, immune-mediated…


  • Take care of the eye! Can reveal the presence of a systemic condition
  • Need to understand where, how and why
  • Few important aspects of the treatment
    • Pain management
    • Try to maintain visual function
    • Aesthetic aspect for pets


Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

F. Ollivier
Clinique vétérinaire d’ophtalmologie
Ophtalmo Vétérinaire Inc.
Montreal, QC, Canada

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