A corneal ulcer is a full thickness break in the epithelium, exposing the stroma beneath. Erosion is loss of some of the 10 to 15 layers.
The majority of epithelial defects in horses have a mechanical etiology, but primary infection with equine herpesvirus does occur less commonly.
Mechanical injury occurs on trail rides, navigating doorways and stalls and everyday life and use. Additionally, sharp or blunt trauma (from rubbing, foreign bodies, grass awns, whips and shanks), high velocity objects (track dirt, corneal drying during prolonged exposed trailering) and following excoriation due to poor eyelid margins (step defect in laceration repair, congenital notch or entropion).
Tear film inadequacies might be considered mechanical if they result in corneal drying by increased evaporation or reduced production or tear spread.
Diagnosis
A brief comprehensive approach to ocular pain or red eye is to first observe for squinting of either eye or defensive behavior on either side, and then examine corneal surfaces with a bright diffuse light. An auriculopalpebral nerve block or sedation permits a safe and complete examination.
If corneal discoloration or a surface defect is present, an aseptically acquired culture swab from the edge of the apparent lesion is performed, and may be later discarded if not required. Fluorescein stain is applied and flushed to remove any excess. Retention is identified more easily with a cobalt filter than with white light.
If corneal edema is substantial, the hydrophilic stroma absorbs less fluorescein and staining is thus less intense. Dimly lit surroundings help. If no fluorescein is retained, but corneal epithelial disease is still suspected, Rose Bengal stain is applied. It is retained if the epithelial-tear interface is abnormal. It is more sensitive for partial thickness epithelial defects (erosions), the fine linear (dendritic) herpes corneal ulcers, damaged epithelial cell surfaces, and also tear film deficiencies, quantitative (reduced production) and qualitative (increased evaporative loss). Rose Bengal has been advocated in diagnosing early fungal keratitis, but is not pathognomonic for that condition.
Examination for foreign bodies should always be performed, including the palpebral conjunctiva and lid puncta. If the ulcer is linear or persistent, a thorough examination of both surfaces of the nictitans may be completed after prolapse under topical anesthesia (proparacaine or tetracaine). Foreign bodies may be small awns or pieces of organic material and insects, or concretions of inflammatory cells, suture or growing hairs. Use extreme caution in removing embedded objects to avoid perforating the anterior chamber or burying them in the stroma.
Normal corneal epithelium is completely replaced every seven to 10 days, so any fluorescein positive lesion that persists longer is either infected, has a persistent mechanical cause or is becoming indolent (failing to heal without an identifiable underlying cause). In fact, most ulcers heal more rapidly and failure to decrease in size should be of concern.
Ulcerative keratitis is not usually infected initially, but worsens rapidly if infection occurs. Flora residing in the conjunctival fornices is one source of infection, but gram negative and gram positive bacteria and fungal spores in the environment may be very pathogenic in the cornea.
Any corneal coloration warrants closer inspection, and implies infection unless it is the diffuse mild graying of corneal edema. All ulcers are treated prophylactically with broad-spectrum or gram-negative-targeted general antibiotics such as triple antibiotic and tobramycin or gentamicin.
The most feared complication of ulceration is keratomalacia, or corneal melting, because loss of mechanical strength during enzymatic digestion of the corneal stroma may progress to globe rupture within 24 to 72 hours. The characteristic opaque gray semisolid appearance hanging from the cornea is diagnostic. Central clearing is of great concern, indicating that stromal thickness is becoming minimal in that area and iris prolapse is potentially imminent (Figure 1, p. 2E). Aggressive medical therapy is necessary to save the globe and vision. Gram stain of cautiously acquired peripheral lesion cytology allows initial antibiotic selection while the culture is pending.
Antibiotic recommendations
Potent topical antibiotics are indicated, which may be either fortified aminoglycosides 1.5% (not 0.3%), compounded cefazolin 5% or fluoroquinolones depending on the Gram stain results. Frequent administration (perhaps hourly at first) aims to sterilize the ulcer rapidly. Uveitis must be controlled with oral NSAIDs and topical atropine. Melting may continue after sterilization because of the intense enzyme release and activation from the microorganisms and the leukocytes that respond. This destructive enzymatic process may be retarded by use of topical serum, EDTA or acetylcysteine.
Researchers at the University of Florida are identifying the enzymes responsible and quantifying response to specific therapeutic protocols. In surgical patients and where uveitis is substantial (thus increasing intraocular drug penetration), oral antibiotics may be of some value. Doxycycline has antibacterial and anti-enzymatic effects, and is my drug of choice for many patients at risk of keratomalacia at a dose of 10 mg/kg PO BID.
Where stromal loss exceeds 50 percent or proceeds despite therapy, surgical intervention is often necessary. A keratectomy and conjunctival flap provide mechanical stability and vascular perfusion at the lesion.
Whenever cosmetic outcome or vision is a priority, early referral is recommended and may avert surgery. Although inflammation is severe, topical NSAIDs are not indicated and may incite melting. Infected ulcers may remain superficial and fail to epithelialize without significant stromal loss. Such ulcers are often noted to have a granular appearance on the surface, and cytology is warranted to better identify the infection. Proliferative plaques on the corneal surface are usually fungal colonies, and are commonly tan or light brown in color.
Fungal plaques may be difficult to control and resolve medically, but a keratectomy is typically curative with or without a conjunctival flap. With appropriate lighting, microsurgical instrumentation and magnification, this procedure may be performed under standing sedation rather than general anesthesia.
Epiphora and lower eyelid swelling concurrent with keratitis and/or uveitis are secondary and rarely indicate the need for nasolacrimal duct flushing. If fluorescein appears at the nostril within five to 10 minutes (Jones test), the duct is patent. Lidocaine gel applied on the distal punctum facilitates catheter placement if necessary. Self-trauma can be reduced with protective masks, and control of ocular pain with atropine/oral NSAIDs.
Contraindications
Topical corticosteroids are contraindicated in corneal ulceration. Eosinophilic keratitis is a proliferative white-gray or pink raised area near the limbus that may retain fluorescein but does not have stromal loss. This specific lesion does require anti-inflammatory therapy, but must be cytologically confirmed before topical steroids are used. Eosinophils infiltrate the cornea and may incite severe keratitis. Although clinically different in appearance than fungal keratitis, inappropriate steroid use may be devastating.
Steroid use is always a dangerous strategy and requires close monitoring. Prophylactic antimicrobials are generally used. Alternatives to topical corticosteroids may also be effective, and be preferable for certain patients. In some localities, eosinophilic keratitis is a seasonally recurrent condition, and the earlier therapy is instituted the less aggressive medication may be.
Source: Tim J. Cutler (2004): Corneal ulcers. In: DVM Newsmagazine April 1, 2004. www.dvmnewsmagazine.com/dvm/
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