9.5 Ophthalmologic Emergencies: Proptosis, Acute Glaucoma, Corneal Perforation & Chemical Injury

Ophthalmologic Emergencies

The AVECCTN blueprint places ophthalmology inside the Misc., Triage/Emergency Care domain, which carries 8% of the examination (~16 items) alongside burns, envenomation, thermal extremes, exotics, and procedures not specific to another body system. Ocular emergencies are disproportionately represented in real emergency caseloads because owners recognize them instantly, and because the window in which vision can be saved is measured in minutes to hours, not days.

The technician's job at the door is to sort the eye that can wait from the eye that cannot, and to avoid the handful of nursing actions that convert a salvageable globe into an enucleation.

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1. Ocular Triage Tiers

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2. Chemical Ocular Injury — The Only "Lavage First" Emergency

Alkaline agents (lime, cement, plaster, drain and oven cleaners) cause liquefactive necrosis: they saponify membrane lipids and continue to penetrate the stroma and anterior chamber long after exposure. Acids cause coagulative necrosis, in which precipitated protein forms a partial barrier — so alkali burns are generally the more destructive of the two.

• Lavage immediately with sterile saline, lactated Ringer's, or the cleanest isotonic fluid available, for 15–20 minutes minimum, using a drip set or a syringe with the needle removed.
• Sweep the conjunctival fornices and behind the third eyelid for retained particulate; dry lime powder must be swept out mechanically, not merely flushed.
• Do not attempt chemical neutralization — an acid-versus-alkali reaction generates heat and worsens the injury.
• Only after lavage: stain, measure pressure if the cornea is intact, and begin topical antibiotic, atropine for ciliary spasm, and analgesia.

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3. Proptosis of the Globe

Proptosis is forward displacement of the globe with entrapment of the eyelids behind the equator, causing venous obstruction, conjunctival strangulation, and progressive corneal desiccation.

Prognostic indicators for retained vision:

• Number of avulsed extraocular muscles. Three or more torn muscles, or an avulsed optic nerve, carries a grave visual prognosis. The medial rectus tears first because it is shortest.
• Pupillary light reflexes. A present direct or consensual PLR is favorable; a fixed, widely dilated pupil with no consensual response to the contralateral eye is poor.
• Conformation. Brachycephalic dogs have a shallow orbit and a prominent globe, so proptosis can follow trivial trauma and is more often reducible with useful outcome. In dolichocephalic dogs and in cats, the deep bony orbit means proptosis requires enormous force — expect concurrent skull, orbital, and intracranial injury and a poor visual prognosis.
• Hyphema, deep corneal laceration, or scleral rupture all worsen the outlook.

Nursing priorities: treat the patient before the eye. Proptosis is a trauma presentation — complete the primary survey, assess for traumatic brain injury and haemoabdomen, and provide analgesia. Keep the cornea coated with sterile ophthalmic lubricant or saline-soaked gauze continuously. Never attempt to replace the globe in a conscious animal; reduction requires general anesthesia, lateral canthotomy, and temporary tarsorrhaphy.

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4. Acute Congestive Glaucoma

Glaucoma is elevated intraocular pressure (IOP) sufficient to damage retinal ganglion cells and the optic nerve head.

• Normal IOP: approximately 10–25 mmHg in dogs and cats by applanation or rebound tonometry, with a normal inter-eye difference of no more than a few mmHg.
• Emergency threshold: pressures above roughly 40–50 mmHg cause irreversible vision loss within hours, not days. A tense, buphthalmic globe with episcleral congestion, a fixed mid-dilated pupil, corneal edema, and obvious pain is congestive glaucoma until proven otherwise.
• Emergency medical bridge:
  • Mannitol 1–2 g/kg IV over 20–30 minutes through an in-line filter — an osmotic agent that dehydrates the vitreous. Contraindicated in dehydration, congestive heart failure, and anuric renal failure; monitor for volume overload.
  • Topical carbonic anhydrase inhibitor (dorzolamide) to reduce aqueous production, often combined with a topical beta-blocker (timolol).
  • Latanoprost, a prostaglandin analog, produces dramatic pressure reduction in dogs by increasing uveoscleral outflow, but it causes intense miosis and is contraindicated when anterior lens luxation or uveitis-induced secondary glaucoma is suspected, and it is largely ineffective in cats.
• Anterior lens luxation — classically in terrier breeds — causes pupillary block and is a surgical emergency; a miotic agent worsens it, which is exactly why latanoprost must not be reached for reflexively.

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5. Corneal Ulceration, Descemetocele & Perforation

Fluorescein staining is the bedside test that stratifies corneal disease.

Melting (keratomalacia) is stromal collagenolysis driven by bacterial and leukocyte proteases; the cornea takes on a soft, grey, gelatinous appearance and can perforate within hours. It is treated with intensive topical antibiotics and anticollagenases (autologous serum, EDTA), often hourly, and it is a nursing-intensive assignment.

Drug rules that appear repeatedly on specialty examinations:

• Topical corticosteroids are absolutely contraindicated in any fluorescein-positive eye. They inhibit re-epithelialization, potentiate collagenase activity, and promote infection.
• Topical NSAIDs also delay epithelial healing and may worsen melting; use with caution and only when directed.
• Atropine relieves painful ciliary spasm and stabilizes the blood-aqueous barrier, but it reduces tear production — avoid it when keratoconjunctivitis sicca coexists, and never use it when glaucoma is suspected.
• E-collar on arrival. Self-trauma converts a treatable ulcer into a perforation faster than any pathogen.

Restraint rules with a fragile or perforated globe: no jugular venipuncture, no neck leads or tight collars, no pressure on the eyelids, no tonometry, and keep the head elevated. Anything that raises episcleral venous pressure can express intraocular contents through a compromised cornea.