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Corneal disease is the major source of ocular pain in horses.
Corneal disease is the major source of ocular pain in horses.
Ulceration is the most common corneal problem and frequently poses a substantial threat to vision, because subsequent infection can rapidly lead to devastating and painful ocular disease. 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.
Improved understanding of common eye condition translates to enhanced case management
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.
Figure 2: Axial corneal ulcer in a recumbent type foal; these ulcers are worsened by exposure and absent corneal blink.
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.
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.
Figure 3: An indolent corneal ulcer with poorly attached and undermined corneal epithelium. Stromal loss is not a feature of these ulcers. Note the eyelid coloboma, which is adjacent to the ulcer when the globe is in its neutral position. An inadequate tear film meniscus resulted in excess tear loss.
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.
High risk corneal diseases: when/what to do next
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.
Occasionally, particularly in the southern United States, infected corneal ulcers may epithelialize before sterilization of the microorganisms and result in a stromal abscess. The abscess is a white-tan color with a complete epithelial lining, which encapsulates the infectious process and the inflammatory response within the stroma. Deeper opacities are frequently fungal in etiology, and may be difficult to manage.
Surgical extraction and corneal transplantation are highly effective, but should be performed early for the best outcome. Use of oral antifungal drugs such as itraconazole (3 mg/kg PO BID administered immediately prior to feeding; available compounded by Wickliffe Pharmacy in Lexington, Ky.) assists in medical management. Oral antibiotics may also be useful for more superficial abscesses, especially in vascularized corneas or when uveitis is significant.
Uveitis management is even more critical in stromal abscess cases, and failure to control it may result in blindness despite resolving the abscess. Consultation about management and consideration of surgical intervention may dramatically improve visual outcome.
Vision may be retained in up to 95 percent of cases with corneal transplant, with healing times reduced from several months to an average of 24 to 28 days with the posterior lamellar keratoplasty procedure (PLK). The PLK is a partial thickness transplant that is performed in the internal corneal layers, while preserving the surface cornea in a trapdoor approach. In contrast, medical management alone has resulted in enucleation rates of up to 50 percent together with prolonged recovery times. Failure to rapidly improve within days is a good indicator for referral.
Foals have additional management issues. Because they are born without a corneal blink response, the cornea is subject to increased trauma in the first one to two weeks of life, or potentially longer in debilitated recumbent foals. Corneal sensation is also poorer in foals than adults. Axial bilateral superficial ulcers are commonly encountered, and typically result from trauma and exposure (Figure 2, p. 4E).
In addition to therapies already detailed, protecting the tear film is helpful. Collagen shields may be used, but are hard to maintain in position and are digested in 24 to 72 hours. Daily fluorescein staining is highly recommended in recumbent or ill foals, because ulcers are so common, and potentially so rapidly progressive. Entropion may occur from dehydration, eyelid trauma or be congenital. If eyelid hair abrades the corneal surface repeatedly, temporary eyelid tacking with 4/0 silk in a vertical mattress pattern is necessary. Sutures should be partial thickness, begin 3 to 4 mm from the eyelid margin, travel perpendicularly and be tied only after all sutures are placed to ensure equal tension.
Other inciting causes for ulceration in foals include facial nerve paralysis, and prolonged recumbency and trauma with hypoxic ischemic encephalopathy or seizures. Congenital abnormalities may be observed rarely in young foals, and include dermoids (skin within the cornea, sometimes haired) and scarring on the endothelium from PPMs (non-painful and fluorescein-negative).
Corneal edema may induce or complicate corneal ulcers, and require additional strategies. Causes of edema include uveitis, endotheliitis, glaucoma, direct blunt trauma (whip injury), chemically-induced and prolonged ulceration. If edema worsens, corneal bullae result from coalescing fluid pockets, and rupture to cause multiple small ulcers.
The equine tear film is often overlooked. Dry eye is rare in horses compared to its frequency in dogs, but it occasionally occurs with sulfa drug use. More commonly, tear film quality is the abnormality. Inadequate tear quality permits more rapid tear loss or failure to coat the corneal surface allowing epithelial exposure and drying. Recurrent superficial ulcers may result (Figure 3, p. 4E). Lower eyelid margin defects, either congenital colobomas or previous eyelid injuries, may increase the risk by preventing the retention of a normal tear film meniscus and tear film spread with blinking.
Other potential causes of ulceration must be excluded before treating an ulcer as healing inadequately or indolent. A characteristic of this poor healing is loose and easily undermined epithelial edges, which are readily shed. Tear supplementation may allow healing with minimal surgical intervention. Viscous tear replacers such as Adequan in artificial tears, refrigerated serum, or commercial products like HylaShield and I-drops may permit healing.
Consider all causes
A report from North Carolina State University demonstrated that surface debridement of indolent-type ulcers with dried cotton-tipped applicators is at least as effective as minor surgery in achieving healing. If the ulcer still persists, a grid keratotomy may be required, but great caution is warranted because infectious agents may multiply rapidly if seeded into the corneal stroma, and there is some risk of iatrogenic corneal perforation. Grid keratotomy should not be performed where stromal loss is evident because such ulcers exhibit different pathologic reasons for non-healing.
Corneal ulcers remain the most common eye problem in horses. Our current understanding of pathologic processes is now much improved, permitting more clinical cases to be managed in the field, and permitting improved outcome in cases that require referral to maximize vision preservation. Your local ophthalmologist is a good resource, together with the color atlas and pocket-sized book listed below.
Dr. Cutler is associated with the Animal Eye Specialty Clinics in West Palm Beach, Deerfield Beach and Wellington, Fla. He is board certified by the American College of Veterinary Internal Medicine and by the American College of Veterinary Ophthalmologists. He received his veterinary degree from the Veterinary College of Ireland, University College Dublin, and his MS degree from the University of Florida. His interests include equine corneal disease and surgery, particularly transplantation. Visit his clinics' Web sites at www.animaleyedocs.com and www.earthlink.net/animaleye.