Chapter 9
Cornea

Anatomy and Physiology

Gross Anatomy

The cornea is not perfectly round; in most species the vertical dimension is shorter than the horizontal (this difference is marked in the ungulates). Nocturnal animals generally have relatively larger corneas than diurnal animals, presumably to allow more efficient light collection. In all species the cornea has less surface area than the sclera. In cats and some ungulates the cornea is relatively large so that all that is seen in the palpebral fissure is cornea, whereas primates generally have smaller corneas in relation to their globe size, allowing sclera to show in the palpebral fissure.

The corneal thickness is different from species to species; its thickness varies from one region of the cornea to another, generally being thicker peripherally than centrally. The reason for providing this information here is because you will be dealing with corneal ulcers and, possibly, biopsies of corneal lesions. You need to be aware of what latitude you have. The general thicknesses in various species are as follows:

• Dog - slightly less than 1 mm
• Cat - about 0.7 mm
• Horse - varies from 0.6 mm centrally to 1 mm at periphery
• Cattle - about 0.8 mm
• Sheep - about 0.75 mm
• Pig - slightly less than 1 mm

The junction between the cornea and the sclera is called the limbus.

Sensory nerve supply - trigeminal, which gives ophthalmic branch which goes to ciliary ganglion and then to cornea; very rich, extensive plexus under epithelium and in superficial stroma. This is reason why superficial ulcers are more painful than deeper ones.

Microscopic anatomy

The cornea normally is avascular. Nourishment is primarily from perilimbal capillaries and aqueous humor.

Anterior epithelium - several cell layers thick (5-20 depending on species), continuous with the conjunctiva. Columnar cells are at the base and gradually become stratified squamous at the surface. Normal epithelium constantly is desquamating at the surface and is completely replaced every 4 - 8 days.

The epithelium is the main barrier to penetration by microorganisms and certain noxious agents. The epithelium easily is abraded; its removal results in marked permeability of the stroma. The peripheral epithelium normally may contain melanin in several types of animals including ungulates and primates.

Bowman's layer - this is well developed only in certain primates, and some cetaceans and pinnipeds. It is not present to any great degree in domesticated animals. It is important in humans in that wounds to the cornea which do not penetrate further than Bowman's layer leave no scar; if Bowman's layer is perforated, scarring will occur.

Stroma (substantia propria) - this constitutes at least 90% of the cornea in most species. It is composed of densely packed, highly ordered collagen fibers. Within this collagen matrix are scattered keratocytes which can effect repair of stromal damage, but over a prolonged period. Capillary loops from limbal blood vessels invade the periphery of the stroma.

Descemet's membrane (posterior limiting membrane) - this is an elastic collagenous membrane which is the basement membrane of the corneal endothelium. At the periphery, it splits into a part that covers the corneal stroma and a part that blends in with the pectinate ligament in species who have this structure. Descemet's membrane is somewhat resistant to penetration by various microorganisms.

Posterior epithelium (also known as endothelium although it does not have endothelial characteristics) - a single layer of cells lining the posterior surface of the cornea. It regenerates much more slowly than epithelium; in some species it does not appear to regenerate, but fills in defects by surviving cells becoming larger.

Although the transparency of the cornea partially is due to the organization of stromal collagen, the endothelium is critical in this respect. These cells keep the cornea in a constant state of relative dehydration; any further imbibition of water would lead to edema and subsequent opacification. The epithelium also must be intact although it does not actively contribute to the relative dehydration.

Physiology

Metabolism

The cornea derives its nourishment via the tear film, the aqueous humor, and the perilimbal capillary loops.

Major function of cornea is the refraction of light; this ability is considerably greater than that of the lens; it requires a clear cornea.

Corneal healing

There are species differences in reactions to corneal insults and in the healing process. The horse shows the most severe reaction and slowest healing, whereas cattle have the least reactivity and heal rapidly (sheep and goats tend to be similar to cattle, but not always). Dogs readily develop vascularization, which tends to speed up the healing process, and increases likelihood of scarring. Cats show relatively little tendency to vascularize, thus healing is prolonged although scarring may be minimal.

Epithelial wounds: These heal rapidly by enlargement and sliding over by adjacent normal cells. If the wound is large enough, there may be mitosis at its edges.

Stromal wounds: These heal more slowly than epithelial wounds. The stromal collagen becomes edematous due to loss of epithelium. Polymorphonuclear inflammatory cells invade the area within hours. Epithelial cells begin filling the defect. If the wound is superficial, it may be repaired in this manner only. Deeper wounds may not be filled completely by epithelial cells and may require stromal collagen deposition (a very slow process - the defect never may fill completely, leaving a thin, epithelialized area or pit).

If the insult is severe enough, or if the healing process is protracted enough, corneal vascularization may occur. Vascularization usually takes a minimum of 3 days to be induced; once started, blood vessel growth may extend into the cornea at the rate of about 1 mm per day. Once blood vessels invade the cornea, they never completely disappear and remain as microscopic 'ghost' vessels, even after the inciting cause no longer is active. An insult to the cornea can render these patent within 24 hours.

Collagenase is an enzyme liberated during corneal wound healing; the source can be from epithelial cells, polymorphonuclear inflammatory cells, keratocytes, or microorganisms. Ordinarily, it is a helpful enzyme in remodeling the cornea during healing. Occasionally, however, it may be excessive and result in severe destruction ('melting') of the cornea. In these situations, such as with alkali burns, many believe the collagenase activity should be minimized or else the cornea may be destroyed before it can heal. Steroids greatly potentiate collagenase activity and are, therefore, contraindicated in most ulcers or similar wounds of the cornea. Collagenase inhibitors are found in the chapter on therapeutics. You should be aware, however, that there is considerable controversy about whether they should be used.

Endothelial wounds and breaks in Descemet's membrane: Endothelium takes a very long time to repair itself. When there is a break in Descemet's membrane, the endothelial cells eventually cover the gap and synthesize a new basement membrane. The time for this to occur differs between species.

Corneal Reactions

Loss of transparency

Definitions

The following terms are just descriptive and are not diseases in themselves; they do not indicate what caused the opacification:

• Nebula - faint change which can be seen with oblique illumination.
• Macula - light gray spot in natural light.
• Leukoma - any dense white spot - this is of clinical importance because it indicates moderate to severe corneal disease. If the spot is associated with adherence of the iris to the posterior corneal surface, it is called an adherent leukoma.

Edema

Edema occurs when the main regions controlling fluid uptake, the epithelium and the endothelium, are disrupted. This appears as variegated gray-blue opacification of the cornea, often referred to as 'cobblestone' in appearance.

The more serious of the two is from endothelial disruption because this is the major source of keeping the cornea relatively dehydrated and clear.

Melanosis

Most pigmentation of the cornea is the result of melanin accumulation. Melanin may be in the epithelial cells following chronic superficial irritation; because of normal epithelial turnover, this melanin may disappear once the noxious stimulus is resolved. In chronic stromal disease, especially with vascularization, melanin will be present in the stroma (in melanocytes); this melanin is of a semipermanent nature because the stroma slowly remodels.

Melanin may be present congenitally, or may migrate onto the endothelial surface from the anterior uveal tract.

Other pigmentation may occur following silver nitrate use in corneal ulcers, or following chronic topical epinephrine use in people.

Corneal vascularization

The appearance of the blood vessels gives clues to their depth, and the condition causing them

Superficial vascularization - has a tree-like branching appearance; is the result of chronic, superficial irritation of the cornea.

Deep (interstitial) vascularization - appears as a deep red rim extending inward from the limbus - the vessels are straight and numerous; signifies severe, deep keratitis or anterior uveitis.

The perilimbal conjunctival blood vessels will become injected whenever there is keratitis.

Congenital Abnormalities

Dermoids

See elsewhere for details.

Congenital anterior staphyloma

Uncommon. Staphyloma is an out pouching (ectasia) of cornea (or sclera) lined by uveal tissue. The lesion generally would appear dark brown or black. Probably caused by embryonic defect. Because these lesions can perforate, they should be repaired surgically: The staphyloma is reduced and a corneal transplant is used to fill the defect. The involved area usually will be markedly opaque following repair.

Congenital inclusion cysts

Occasionally, groups of epithelial cells may become incarcerated in the developing cornea. They appear as an area of opacification, possibly with cystic changes.

These cysts may grow slowly, but usually are not a problem. Can be surgically excised if necessary.

Microcornea

Smaller than normal cornea with otherwise normal globe - usually clinically insignificant.

Seen sporadically in many breeds, but especially in miniature schnauzers. In the latter, the condition is heritable and may be associated with other, more severe problems such as cataract.

Other ocular anterior segment anomalies also may be present, e.g., shallow anterior chamber, persistent pupillary membrane.

No treatment is necessary, but because the condition may be heritable, affected individuals should not be used for breeding.

Acquired Abnormalities

Keratitis

Keratitis is inflammation of the cornea. Along with conjunctivitis, this is one of the most common ocular problems which the practitioner will face. Keratitis has numerous causes, some specific, others incidental or secondary. A diagnosis of keratitis usually must be qualified by stating the predisposing or actual cause because the use of keratitis alone is nonspecific.

General signs of keratitis, regardless of cause:

Pain is one of the most common signs of keratitis. The more superficial the lesion, the more painful it may be because this is where the nerve endings are.

With corneal irritation there is secondary iridocyclospasm. The iridocyclospasm may be severe enough to cause photophobia and blepharospasm. All these may cause self-mutilation.

Lacrimation or excessive tearing - this leads to epiphora. The discharge may become mucopurulent especially if bacterial infection occurs.

Conjunctival hyperemia - the 'eye' appears reddened.

Loss of corneal transparency due to edema, cellular infiltration, vascular ingrowth.

Vision usually unaffected unless keratitis is severe. If severe and bilateral, the patient may have impaired vision. If bilateral severe blepharospasm is associated with the disease, this also would cause temporary loss of vision because of the closed eyelids.

Pannus (chronic superficial keratitis) in German shepherd dogs

There is a subepithelial infiltration of the cornea by fibrovascular tissue and mononuclear inflammatory cells.

When the term pannus is used with respect to the German shepherd, it refers to a specific degenerative disease of probably heritable nature. In these cases the term represents the disease name. However, the term pannus can be used to describe the subepithelial, fibrovascular corneal infiltrate seen in any chronic, superficial keratitis.

About 90% of all cases occur in German shepherd dogs, and shepherd crosses. Also seen in dogs of similar ancestry (Belgian sheepdog, great Dane, boxer, greyhound, and collies), and long-haired dachshunds.

Cause: Unknown - may be related to autoimmune problems (Campbell, et al.). Will be made more severe by irritation (ultraviolet light, dust, wind or infection).

Because ultraviolet light is greater at higher elevations, individuals living at or higher than 5000 feet above sea level may have higher prevalence, greater changes, less response to therapy (Slatter, et al.).

Signs and natural history: Although it almost always is bilateral, it may begin in one eye simulating a unilateral disease; affected individuals usually are older than 9 months and most are first seen between 2 to 5 years of age. It characteristically begins in the ventrolateral limbal region of the cornea as a zone of granulation tissue (pink) invading the cornea. From here it continues to grow inward; as this continues, a lesion may begin in the medial limbal area and grow towards the original lesion. Lesions may then arise from dorsal and ventral limbal areas. Eventually, the entire corneal surface may become involved . Soon after the fibrovascular infiltration begins, melanin is deposited in the affected corneal epithelium and stroma . When enough of the corneal tissue is opacified, the dog may lose vision in that eye; if this occurs bilaterally, the dog may become blind. The progression of changes usually is slow, but can develop within several weeks.

In spite of the corneal changes, the dog usually shows relatively little evidence of discomfort. The client may fail to notice the initial lesion; it may not be until the dog shows signs of vision loss that the dog is brought to you.

Treatment: Treatment can be considered only temporary arrest or control because most patients must be treated continuously (lifelong) or else the problem will recur. Response to treatment is related to environment: control is more difficult in dry, dusty areas or above 5000 feet above sea level.

Although topical corticosteroids are traditionally the most effective form of treatment, some people have tried topical cyclosporine (Jackson, et al.). The latter is considerably more expensive than steroids and seems to offer no advantages.

Early lesions: Use strong steroids such as 0.1% dexamethasone, or 1% prednisolone acetate; drops may be easier for client compliance and may be cheaper. Antibiotic is contraindicated except if there is concurrent infection and then only until infection is resolved.

Initial therapy must be vigorous: 1 drop in each eye 6-8 times a day for at least 2 weeks, or until the granulation tissue regresses (melanin may not disappear, so do not use this as a criterion). Then, you gradually can reduce the frequency to the lowest necessary to prevent recurrence; in some cases, this may be only 1 drop every other day. You should make every attempt to educate your clients so that they can monitor the condition and increase or reduce medication as needed to control the disease. You should have frequent examinations until you are sure the client is adequately controlling the disease; after that, exams once every 6-12 months are probably sufficient, unless the client experiences difficulty.

Moderately advanced lesions or lesions where topical treatment is becoming ineffective: Start initially with a subconjunctival injection of corticosteroid such as triamcinolone. Remember to place medication near the lesion site.

CAUTION - Although Depo-Medrol® (methylprednisolone) has been used in the past, some dogs may have adverse reaction which could lead to loss of the eye and I strongly recommend you do not use it (Fischer). There have been similar problems reported with triamcinolone use (Håkanson, et al.).

Simultaneously treat with topical steroids as described for the early lesions. Should get improvement in less than a week. May need to continue topical therapy at an increased frequency. Also may need to repeat the subconjunctival injection.

Lesions which progress in spite of corticosteroid treatment: Beta radiation may be used in conjunction with steroid injection. Each application site should receive from 5000 to 7500 rads; the perilimbal non-corneal tissue also should be irradiated. Treat only those areas that are affected. Continue topical therapy as described for the early lesions.

You can expect dramatic diminution of the vascularization within a week. Melanin in the epithelium will disappear. However, if there is melanin in the stroma, much of it may never disappear. You can repeat the subconjunctival steroid injection in 2 to 4 weeks. If this does not lead to improvement, you could repeat the beta application about 2 months after the first application.

Cryotherapy also can be tried. You should consult Holmberg, et al. for technique.

Advanced lesions causing temporary vision loss due to severe scarring or melanosis: For these cases a superficial keratectomy may be necessary. This is a specialized piece of surgery which can have serious complications associated with it. The decision whether to do the surgery requires experience and detailed understanding of the underlying problem. Therefore, it would be best to refer the patient to a specialist when you think a keratectomy is the only solution to the problem.

Prognosis and complications: Dogs living at high altitudes, or in dusty conditions, may respond poorly to therapy. The corneal disease may advance despite diligent efforts, and the client may eventually give up. In these cases, the cornea may become densely melanotic and the dog may be blind, but comfortable.

The above notwithstanding, most patients respond well to therapy and the condition is easy to control.

Some corneas will undergo lipoidal degeneration manifested as crystalline deposits. These are of no concern. After surgery, some corneas may undergo cystic degeneration (epithelial bullae may form). These may require further surgery to remove, but often can be ignored.

Because these patients are on chronic topical steroid therapy, they are at greater risk than the average dog if they should suffer a corneal scratch, ulceration or laceration. If this occurs, steroids should be reduced in frequency or discontinued until you are sure adequate healing is taking place.

In spite of all the theoretical possibilities, there appear to be few clinically relevant problems associated with the use of topical steroids for many years in these dogs. There may be suppression of adrenal function due to systemic absorption of the steroids. It is possible that this may have adverse effects on the patient although this seems to be rare.

Pannus as a result of nonspecific, chronic, superficial keratitis

Chronic infection or irritation may result in a lesion similar to German shepherd pannus. When this is seen, be sure to make a thorough examination to find the cause of the lesion. Treatment is aimed at the specific cause and symptomatically at the vascularization (with steroids as for German shepherd pannus). Superficial keratectomy may be necessary to remove scar tissue, only if this tissue interferes with vision. If the primary cause of the lesion is successfully treated, the lesion should not recur.

Corneal granulomas

These uncommon lesions are seen in collies and occasionally in other canine breeds. They are rapidly growing gray-pink masses that occur at the limbal area. They may mimic neoplasia. Although steroids, topical or subconjunctival, may have some beneficial effects, surgical excision usually is necessary. Topical steroids, e.g., 1% prednisolone acetate, should be used 4-6 times a day after surgery; therapy can be discontinued after there is complete healing. They may recur after surgery. The cause of these granulomas is not known.

Melanosis of the cornea

This often is referred to as 'pigmentary keratitis.' However, the deposition of melanin in the cornea is a nonspecific response to irritation. Therefore, the term 'pigmentary keratitis' does not necessarily refer to a specific entity; it describes a complication of a number of diseases. The melanosis usually is superficial.

Occurrence: Any chronic irritation of the cornea (trichiasis, nasal folds, entropion, distichiasis, keratoconjunctivitis sicca, German shepherd pannus), or some injuries may lead to melanosis. Brachycephalic breeds with prominent eyes especially are prone because of corneal exposure (from lagophthalmos) to the environment. Some Pekingese and Pug dogs can develop melanosis with no apparent cause.

Treatment: Remove the cause, if possible. Use strong topical steroids frequently to reduce residual inflammation. Epithelial melanin will disappear, but stromal melanin may be permanent.

Keratectomy should be considered only if the melanin is causing vision disturbance (this is unusual). Often, the surgical site undergoes melanosis after surgery, so that no benefits are derived. If you are considering keratectomy for this problem, you should consult with a specialist to see if another approach would be better. There is greater than usual risk of corneal perforation when keratectomies are done on prominent-eyed dogs.

Prognosis: If the cause is found and removed, prognosis is good. In many situations, however, a cause is not apparent and topical steroid therapy may be necessary indefinitely to delay or prevent progression of the melanosis.

Superficial punctate keratitis

Characterized by epithelial and subepithelial infiltrates. These tiny, white dots give the cornea a stippled appearance. The disease usually is limited to the central part of the cornea and the opacities may spontaneously disappear in 6 - 12 months. The cause is unknown.

Treatment usually is not indicated because the patient is not in distress and the disease spontaneously subsides. If a problem occurs, may try topical steroids to reduce inflammation.

Corneal necrosis (corneal sequestrum, corneal nigrum)

In this uncommon condition, a focal region of cornea turns dark brown and is associated with death of the tissue. It is seen almost exclusively in cats (Morgan). Although it is seen spontaneously in the Persian breed, it can occur in virtually any cat secondary to chronic corneal disease such as ulcerative keratitis, keratitis secondary to entropion, or exposure keratitis due to eyelid agenesis.

The cause of this condition is unknown; nor is it known why it does not occur consistently in the situations known to precipitate it.

Affected individuals often show no significant signs of discomfort in the spontaneous cases; the underlying corneal disease in secondary cases dictates the signs seen.

Fluorescein may be taken up at the edges of the lesion where corneal epithelium may be absent; the lesion itself does not stain.

Treatment is aimed at the primary cause, if applicable. Once the primary cause is resolved, the cornea may extrude the necrotic area over a period of weeks to months. In spontaneous cases, treat with a steroid preparation (add antibiotic if there is ulceration) for several weeks to see if the lesion will be extruded. This may slow extrusion, but I think it may be important in that it may reduce inflammation and improve the comfort of the patient.

In those cases, primary or secondary, in which extrusion does not occur or in which the patient displays discomfort or pain, the lesion should be removed by superficial keratectomy. You first must evaluate the depth of the lesion because a few may be too deep to remove surgically, or the cornea may be thin in the center (where it is not visible) in which case you may cause perforation. Because of the potential for complications, this surgery should be referred to someone who has an interest and the appropriate equipment. After surgery, the eye is treated as any corneal ulcer would be treated.

Interstitial keratitis

This is not a specific disease, but represents the involvement of the entire cornea by severe inflammation. Many situations can develop into an interstitial keratitis: secondary to non-ocular disease (canine distemper, tonsillitis), trauma, invasion by infectious agents, or association with anterior uveitis.

Because the entire cornea is involved, edema is diffuse and severe; the edema may be severe enough to change the contour of the cornea and prevent visualization of deeper structures; epithelial bullae may develop. Deep and superficial vascularization is prominent. Signs of uveitis are present even in those patients not having primary uveal disease. Hypopyon often is present.

Treatment: Must be aimed at the primary cause, but also at minimizing the damaging effects of the corneal inflammation; and because uveitis is present, this must be addressed:

Topical atropine - produces iridocycloplegia as well as providing pupillary dilatation.

Dilating the pupil reduces the chance for synechiae in the visual axis.

Iridocycloplegia reduces pain by relieving the iris and ciliary spasm seen with the anterior uveitis.

Steroids - strong, topical (do not use if ulcerated) 4-6 times a day; systemic use of steroids usually is not necessary nor desirable.

Antibiotics - ideally should first determine if there is infection, otherwise use a broad spectrum one topically in concert with the steroids; systemic use usually not necessary nor desirable.

After the cornea starts to clear, continue only the steroids until there is no more inflammation.

Prognosis: Long term relief depends on the underlying cause. However, you can expect that there will be slight to severe permanent corneal opacification due to scarring. In most patients, this will not have an observable effect on vision. If vision is diminished, treatment modalities such as superficial keratectomy or corneal transplants could be considered, but usually are not rewarding.

Ulcerative keratitis

A corneal ulcer is the loss of corneal epithelium or stroma. A variable amount of inflammation (keratitis) always accompanies corneal ulceration (Nasisse).

Causes:

Mechanical: abrasions by clippers, whips; eyelash abnormalities; foreign bodies; exposure of cornea in proptosis or prominent-eyed breeds; eyelid diseases such as entropion.

Infections:

Bacterial - Pseudomonas especially is serious; Moraxella in cattle.

Viral - canine distemper, herpesvirus (Nasisse), infectious bovine rhinotracheitis.

Mycotic - numerous species, horse most commonly affected.

Chlamydophila.

Neurotrophic: Non-function of ophthalmic branch of trigeminal nerve. Diagnosed by lack of corneal sensitivity and usually a history of recent trauma to head. The ulcer does not arise simply due to lack of innervation, but may be the result of trauma to an eye which has lost an important defense mechanism against corneal irritation, the blink reflex.

Metabolic disturbances: Conditions such as hypoestrogenism (e.g., in ovariohysterectomized dogs) have been purported to be associated with some spontaneous ulcerations, but this has not been proven.

Signs:

Pain - manifested by blepharospasm. Most ulcers are extremely painful. There also is reflex iris and ciliary spasm in almost all cases so that the corneal pain is compounded by anterior uveal pain; photophobia occurs as a result of this.

Discharge - usually serous at first, then may become purulent.

Edema - most ulcers have considerable edema which extends a short distance beyond the edges. Descemet's membrane, however, will not become edematous; thus, if the central region of an ulcer begins to clear, it may not be a favorable sign because it may represent deepening of the ulcer. Certain superficial erosions, such as in the boxer dog, remain relatively clear (Gelatt and Samuelson).

Changes in contour of cornea - if the ulcer is deep, an excavation readily is recognized; if the ulcer is superficial, it may not create a noticeable change in contour.

Vascularization - whether this occurs depends on the nature of the lesion and the length of time it is present. Some lesions, such as superficial erosions in various canine breeds, do not seem to incite vascularization regardless how long they are present.

Diagnosis: Thoroughly examine the eye to find a cause for the ulcer. If none is found, then must assume the ulcer is traumatic from non-ocular sources.

Use fluorescein dye to outline limits of ulcer . Be sure to use only a tiny amount of fluorescein and examine the eye soon after putting in the dye or else excess dye will obscure things and the stain will extend well beyond the actual border of the ulcer due to migration through the stroma .

Superficial ulcers may not be visible without fluorescein. It is, therefore, imperative to use fluorescein routinely in painful eyes when a cause for the pain is not evident.

Fluorescein also is useful in monitoring healing progress because it does not stain epithelialized areas.

Treatment: Should be continued until the ulcer is healed.

Correct the cause if known.

Topical medical treatment for most ulcers: Minimize chances for infection - drops may be better than ointment because of less interference with healing.

Bacterial: Although you could culture and do a sensitivity test, most ulcers are not the result of a primary infection. Thus, a broad spectrum antibiotic usually is sufficient to prevent infection by opportunistic bacteria. Treat 4 times a day.

For ulcers caused by Streptococcus in the horse, penicillin usually is the drug of choice. Because no ocular preparation currently is available, you will have to make it up. Remove 3 ml from a 15 ml bottle of artificial tears and place in 1 vial of penicillin G succinate (5 million units); mix and then place the reconstituted penicillin into the original artificial tear bottle (Brightman); use this at least 6 times a day initially.

Viral: Can use idoxuridine or vidarabine. Follow instructions on the label. See other literature for more information (Nasisse a, b).

Mycotic: See elsewhere for details.

Chlamydophila: Chloramphenicol or tetracycline traditionally used; erythromycin may be beneficial.

Relieve pain caused by iridal and ciliary spasm - use an iridocycloplegic - 1% atropine 3 or 4 times a day for 2 - 3 days, then once or twice a day.

Iridocycloplegia also results in pupillary dilatation; this action is helpful because it reduces chance of synechiae in visual axis and because it provides a means of monitoring the effectiveness of therapy: if the pupil is well dilated, there probably is adequate iridocycloplegia.

Anticollagenase agents

Use only if the ulcer shows signs of rapid progression. Acetylcysteine is available commercially, however serum from the patient may be used. Treat 3-4 times a day with either. There is considerable controversy as to whether these agents are beneficial in corneal ulcers.

Subconjunctival injection: This should be used only when an infection is present and is the reason for an ulcer's lack of healing. In these unusual situations, the antibiotic of choice can be injected.

Sometimes it is more effective to give an iridocycloplegic subconjunctivally initially and follow with topical treatment. This particularly is true with horses because of the intense iridocyclospasm (and resulting pupillary constriction) they have with uveitis.

Protect the cornea: If the ulcer is deep or is slowly healing, or there is the chance of self-trauma, it may be prudent to 'bandage' the eye. These techniques may speed the healing rate of all ulcers and give additional mechanical support to the cornea in the case of deep ulcers. However, they are not routinely indicated nor necessary.

Soft contact lens: The simplest way to provide some protection is through the use of a soft contact lens (Dice and Cooley; Fink, et al.). You may be able to obtain these at minimal or no cost from human ophthalmologists, optometrists or suppliers if you ask for those which are 'expired.' The dioptric power is not important, but the diameter should be large enough to cover most of the corneal surface, if possible. You also can purchase these lenses specifically made for veterinary use.

Third eyelid flaps: The third eyelid may be sutured to the bulbar conjunctiva or to the upper eyelid. You will need general anesthesia. Do not do in birds because this will damage the third eyelid, and the third eyelid is critical for corneal health in birds. (Do a tarsorrhaphy if you need to provide temporary corneal protection in a bird.)

Use horizontal mattress sutures of braided non-absorbable type (4-0 to 6-0 for small animals; 2-0 to 4-0 for large animals). Leave the suture ends 5-10 mm long.

Although some people suture the third eyelid to the bulbar conjunctiva, the preferred method is to suture it to the upper eyelid .

Before placing any sutures, establish where the fornix is by using the blunt end of a scalpel handle or similar instrument. This is the site where the leading edge of the third eyelid should come to when you finally tie the sutures. Be sure to grasp the leading edge of the third eyelid and pull it across the globe to observe its normal plane of movement, and to rule out abnormalities, such as adhesions, which would preclude doing the surgery. Your sutures must be preplaced, and you should use buttons, plastic tubing (split lengthwise) or piece of rubber band to support the sutures where they contact the skin. Be sure to go through the support material before you go through the skin for your first suture at each site. The sutures should be placed several mm from the leading edge of the third eyelid, and should go no more than half-thickness, entering from the palpebral surface. You should strive to include cartilage to give added strength. Bear in mind that there always is the risk of corneal abrasion, particularly if the sutures begin to give out and the third eyelid starts coming down.

You may have to do a temporary partial tarsorrhaphy to minimize tension on the flap.

Remove sutures in 7-14 days if they have not pulled out before then.

Tarsorrhaphies: See elsewhere for technique.

Conjunctival flaps : Should be used when the ulcer is very deep. See elsewhere for techniques.

Cauterization: Superficial ulcers which are refractory to topical medication or which re-epithelialize only to break down again may need to be cauterized. The rationale behind this technique is that dead and dying epithelium (which interferes with healing) is removed allowing 'fresh' epithelium to grow and produce healing.

Cotton tipped applicators are lightly soaked in cauterizing solution (2% tincture of iodine is best) and, after corneal anesthetization, the edges of the ulcer are gently rubbed to remove the epithelium. Also may use the cotton tipped applicators without the cauterizing agent.

Forceps are used to pick up and remove loosened epithelium . Rinse the eye with artificial tears when done and treat medically as above.

Osmotic agents: In some cases where healing is slow, some people have advocated the use of topical 5% NaCl ointment 3-4 times a day. This may be helpful in cases where the epithelium fails to become adherent to the underlying stroma, but there is no proof that it works.

Systemic medication: In the case of deep ulcers, or where sealed perforation of the cornea is suspected, or where there is evidence of concurrent uveitis, systemic administration of broad spectrum antibiotics for several days is indicated.

Granulation tissue associated with deep ulcers: It is not uncommon to have granulation tissue fill a deep ulcer. Although it appears objectionable, granulation tissue should be encouraged in these cases because it results in the first stage of the healing process. Once the ulcer is filled, topical corticosteroids should be used 3-6 times a day to reduce scar formation. After a couple weeks, the eye should be quiet and the medication can be discontinued to see if there is resolution; continue therapy if there is reoccurrence of granulation tissue.

Whenever the cornea heals in this manner, a scar of various proportions will result. This usually is of no concern, but cannot easily be treated in any event in our patients.

Refractory superficial ulcers: Most corneal ulcers heal rapidly once the cause is removed and appropriate medical therapy is provided. If a superficial ulcer does not heal within 7-14 days, the patient should be re-evaluated carefully. Sometimes, more diagnostic tests are necessary; usually, however, it is just a matter of providing eye protection or removing loose epithelium at the edge of the ulcer. If there is no evidence for infection, do not continually change antibiotics because healing has not occurred; antibiotics do not heal the cornea, they only minimize invasion by bacteria. Nothing currently available 'heals' ulcers; we simply protect the eye while natural bodily processes work.

Deep corneal ulcers: Most of the previous discussion primarily has been concerned with uncomplicated, relatively superficial ulcers. In cases where the ulcer deepens or is the result of a deep wound, there is the danger of corneal perforation and its associated problems.

Treatment of deep ulcers which do not appear to be in immediate danger of rupture: You may elect to treat these conservatively, especially when the patient is quiet and there is evidence of a good attempt at healing (i.e., vascularization).

Support the cornea by either a third eyelid flap or a tarsorrhaphy; leave in place for 7 - 14 days. If the cornea ruptures, remove the sutures early; rupture may be suspected if the eye is sunken, if there is considerable increase in ocular discharge, if the eye becomes more painful to the patient, or if there is blood in the ocular discharge.

Treatment of deep ulcers 5 mm or less in diameter, with danger of rupture: Debride the edges of the ulcer and do a third eyelid flap. Leave up for 14 days. If flap begins coming down before this time, remove its sutures.

Topical medication as previously described.

Systemic antibiotics for 5 days may be indicated.

If there is any question on treatment, refer the patient to a specialist.

Treatment of large, deep ulcers in which perforation is imminent: Use a conjunctival flap (grafts of conjunctival or corneal tissue also can be done [Hacker; Scagliotti]). This may be better than third eyelid flaps or tarsorrhaphies because it brings a blood supply directly to the lesion.

This should be done utilizing only the conjunctiva; you will have to be careful during dissection so that you do not produce a thick flap. An ophthalmic surgery book should be consulted for more details on technique.

After surgery, the flap will become adherent to the ulcer bed, but not to normal corneal epithelium. In about 2-3 weeks, the flap can be trimmed away.

Peripheral flap. Refer to illustration and instructions for technique . After surgery, treat topically or systemically, or both, depending on the seriousness of the eye lesions. When healing has occurred, trim the flap around the original ulcer - the remainder of the conjunctiva usually will slide back to the limbus and re-attach spontaneously (if it does not, suture it to the limbus using 6-0 absorbable suture). At this point treatment with topical steroids is indicated to reduce scarring.

Total conjunctival flap. Refer to illustration and instructions for technique .

Descemetocele : When an ulcer becomes very deep, normal intraocular pressure may cause Descemet's membrane to protrude through the wound. A small, transparent vesicle will be seen and is termed a descemetocele. Treatment is aimed at supporting and protecting this lesion until the cornea can heal. There are various surgical procedures which may be helpful, but these generally should be done by a specialist. Unless the descemetocele is less than 3 mm in diameter so that a conjunctival or third eyelid flap may work, the patient should be referred to a specialist.

Some surgeons recommend doing an anterior chamber paracentesis to lower intraocular pressure as part of the therapy. The rationale behind this is faulty for several reasons: 1) intraocular pressure usually is lower than normal in these cases due to concurrent uveitis, 2) aqueous removal lowers intraocular pressure for only a few minutes after which time new aqueous has re-stabilized the pressure, 3) there is the risk of introducing infection, and 4) there is the risk of causing intraocular damage with the needle.

Perforating ulcers with prolapse of iris: Generally, these require special instrumentation and experience to treat. Refer the patient to a specialist.

Boxer ulcers (recurrent corneal erosion)

Occurrence: Seen mostly in boxer dogs over 5 years of age. Usually unilateral, but may be bilateral or alternate from eye to eye.

Although most common in boxer dogs, also occasionally seen in Boston terriers, Chihuahuas, poodles, and some horses.

Pathogenesis: The condition appears to be due to a defect in epithelial basement membrane which prevents the epithelium from becoming adherent to the superficial stroma.

Signs: Mild to moderate pain with epiphora.

Cornea usually remains clear except in region of ulcer.

Minimal to no vascularization of the cornea.

Treatment: Consists of removing loose epithelium (mechanically or by cauterization) and then treating as a mild, superficial ulcer (see previous sections).

Hormone therapy sometimes is recommended for spayed female and old male dogs. For spayed female dogs, use oral estrogen replacement at 1 mg every 3-4 days. The rationale is that estrogens are essential for epithelial health and healing. Oral testosterone in old male dogs may assist healing of these ulcers. In neither case, however, is there conclusive evidence that hormone therapy is helpful.

Prognosis: These ulcers are recurrent. A permanent 'cure' is unusual and you should warn the client to expect recurrence in same eye, or new ulcer in unaffected eye. These recurrences may be weeks to many months apart (sometimes years).

Fortunately, prompt treatment may result in quick healing and permanent corneal damage is unusual.

Eosinophilic keratitis

This is an uncommon condition in cats (Morgan, et al.), although it has been seen rarely in the dog and horse. It is characterized by corneal infiltration with eosinophils, mast cells, or both. A granulomatous inflammatory response is seen. Vascularization of the cornea ranges from mild to a thick mass of granulation tissue covering most or all the corneal surface. The lesion usually originates from the lateral or medial aspect of the limbus. Adjacent bulbar conjunctiva or nictitating membrane occasionally may become involved. Loss of corneal epithelium is not common, and pain often is not a feature of the condition.

There does not seem to be any age, gender, or breed predilection. Although often unilateral, both eyes can be involved , especially if treatment is ineffective.

Diagnosis is made by cytologic exam of scrapings of the corneal lesion, or by superficial corneal biopsy. In both cases, the presence of eosinophils, mast cells, or both is considered diagnostic (assuming other causes of mass lesions of the cornea have been ruled out; e.g., there could be infiltration of the cornea by a limbal mast cell neoplasm).

Treatment initially is comprised of topical strong steroids, such as prednisolone or dexamethasone, given several times a day. If the patient responds positively, the dose can be reduced until a maintenance level is found. If this is unsuccessful, oral megestrol acetate may be tried. The dose can be started at 5 mg every 24 hrs for five days, followed by 5 mg every other day for 10 days, tapering off as the lesion regresses. Because of the potential for serious side-effects, the use of megestrol acetate for extended periods should be avoided. Nor should topical steroids and megestrol acetate be used simultaneously because this may exacerbate adrenal suppression.

The prognosis for clearing of the lesion and continued remission must remain guarded. Although some cats have had remissions that have lasted as much as a couple years from one treatment period, some have recurred despite therapy. See Paulsen, et al. for more information on patient management.

Mycotic keratitis

Although uncommon, it is extremely serious. Seen much more frequently in horses than in other species (Marlar, et al.).

Cause: The most common predisposing factor in mycotic keratitis in all species is the use of topical corticosteroids in cases of corneal ulceration. The pathogenesis appears to be the reduction of local immune mediated responses so that normally saprophytic fungi and pathogenic contaminants are afforded an opportunity to proliferate. The additional use of antibiotics reduces the bacterial flora thereby reducing the competition between bacteria and fungi for substrate. However, when antibiotics alone are used, fungal infection does not appear to be a problem.

Primary mycotic keratitis does occur, but most mycotic keratitis is secondary to some form of trauma to the cornea.

Some of the fungi that can be found include:

Candida - moderately pathogenic. Present in conjunctiva of some normal eyes.

Aspergillus - moderately severe. Seen frequently.

Fusarium - uncommon, but severe.

Alternaria - moderate pathogenicity.

Mucor - low pathogenicity.

Others - most fungi might be able to take advantage of a situation in which corneal health has been compromised.

Signs: There are no pathognomonic signs; affected individuals show eye signs and behavior similar to that caused by any other keratitis or ulcer. However, some affected corneas have a creamy appearance to the site, or there may be lines of inflammation radiating from the main focus of inflammation. There often are satellite lesions in the cornea. Most of the individuals exhibit more pain than you would expect judging from the extent of the lesion.

Diagnosis: Horses (or, rarely, others) with refractory ulcers or keratitis, especially those who have been on topical corticosteroids, should be suspected of having mycotic keratitis.

Take scrapings from the edges of the corneal lesion; stain with Gram's or Giemsa stain and examine for fungal elements; make several slides and examine all before considering negative. If there is epithelium over the lesion, debride the epithelium before taking scrapings.

Culture. Blood-agar or Sabouraud cultures at room temperature and 37° C; keep at least 2 or 3 weeks before considering negative. Growth may appear in a few days in some cases.

Treatment: As soon as you know you are dealing with a fungus, institute antifungal therapy. Although it would be best to use a specific agent (Coad, et al.), you often will not know which fungus you are dealing with for several days or weeks. In these instances, it is best to begin with either topical miconazole, nystatin or amphotericin B until you get more information on the organism, or the condition disappears. Absolutely no corticosteroids should be used. Miconazole (Monistat i.v.®) is particularly useful because it is a solution and is easy to use with subpalpebral lavage systems in the horse.

Prognosis: If the course has been chronic, there may be some hope in finding the agent, treating it specifically and saving the eye. Treatment must be vigorous - subpalpebral lavage system with hourly treatment for several days followed by less frequent daily medication for several weeks may be necessary.

If fulminating, the eye may be destroyed before the agent is identified or before an antifungal agent is effective.

Infectious bovine keratoconjunctivitis ('pink eye') (George)

Occurrence: Usually in groups of cattle, healthy or debilitated; worldwide; usually spring and summer (reflects activity of the face-fly, Musca autumnalis - important in the spread of the disease).

Morbidity high (up to 50% in mature herd, 90% in calves) - no mortality, but primarily a loss of condition - loss of weight or lack of weight gain, or loss of milk production.

Brahma cattle may be less susceptible.

Signs:

Lacrimation and epiphora

Photophobia

Swollen eyelids, blepharospasm

Keratitis, conjunctivitis, corneal edema - may progress to ulceration, perforation, collapse of anterior chamber - may lead to severe anterior uveitis

Pathogenesis: Ulcer and edema begin centrally in majority of cases - edema may eventually involve entire cornea - may regress from this point or continue to progress (most regress).

If progresses, get superficial vascularization from limbus, ulcer becomes deeper, abscess forms in center of cornea - deeper vessels invade the cornea and anterior uveitis occurs; get appearance of a red or pink cornea with a white center - may get perforation and iris prolapse . In either situation, most cases eventually resolve spontaneously in several weeks to months - blood vessels wall off the abscess and eventually it becomes smaller and necrotic material is extruded. If iris is present in wound, usually get anterior synechia or adherent leukoma ; may also get posterior synechia and focal, non-progressive cataract. Outcome of all this in most cases is good vision with minor corneal scar; severe cases may become glaucomatous due to angle blockage from iris adhesions.

Usually, but not always, bilateral.

General course - 2-5 weeks in young, less in older.

Cause: Moraxella bovis is the bacterium most commonly found and generally is accepted as cause - gram negative rod, pleomorphic - hemolytic or non-hemolytic colonies.

Produces endo- and exotoxins which cause intense coagulation necrosis of cornea.

Piliated form generally is the disease producer, but there are some piliated forms that may be avirulent.

Modifying factors:

Ultraviolet light causes non-hemolytic form to become hemolytic.

Infectious bovine rhinotracheitis virus enhances pathogenic effect by creating more suitable environment, possibly by virtue of the conjunctivitis it produces.

Differential considerations: Malignant catarrhal fever - generalized corneal opacity, systemically ill.

Infectious bovine rhinotracheitis - conjunctivitis, peripheral corneal opacity, but usually no ulceration - also have respiratory signs.

Parainfluenza - minor conjunctivitis - respiratory signs predominate.

Any cause of keratitis or conjunctivitis, e.g., grass awns, trauma, etc.

Treatment: Almost any antibiotic will shorten course (George, et al.) - steroids also are beneficial. This is one of the few situations in which topical steroids may be used even if there is corneal ulceration.

For early or less severe cases, just topical application of an antibiotic-steroid compound. Some have used antibiotics in the form of collagen inserts for minimum handling of the affected individuals (Punch, et al.).

For severe cases or those refractory to topical medication - subconjunctival injections of 1:1 combination of antibiotic (e.g., neomycin or penicillin) and steroid (e.g., dexamethasone) - may have to be done several times, a few days apart - continue topical medication at same time. Topical atropine (1-2%) also should be used several times a day for iridocycloplegia. Do not mix an aminoglycoside antibiotic with a penicillin antibiotic because the aminoglycoside may be inactivated by the penicillin.

Protection from the sun should be available.

For severe ulcerations or perforations, a modified third eyelid flap is recommended in addition to medical therapy (Anderson, et al.).

Because healing eventually would occur spontaneously in most cases, the main objective of treatment is to get the patient to feel better as quickly as possible so that economic losses are kept to minimum.

Intramuscular injection of long-lasting oxytetracycline may be an effective treatment (20 mg/kg body weight); give 2 injections, 3 days apart.

Control and prevention:

Fly control.

Dust control - bacteria are carried in fomites.

Recovered individuals have some degree of resistance to reinfection.

Vaccination - vaccines are available; one product is called BovEye® by Norden, and another is Piliguard®Pinkeye-1 by Schering; you should be aware, however, that some workers have found that the vaccines were not effective in reducing the number of calves becoming infected nor the severity of the disease (Smith, et al.).

Corneal dystrophy

Corneal dystrophy should be used only to describe a condition which is primary to the cornea, is slowly progressive or stationary, is bilateral and fairly symmetrical, is heritable, and is not accompanied by inflammation or vascularization. The cause for corneal dystrophies rarely is known. In most cases, there is deposition of material, often lipoidal, in the various layers of the cornea. In human patients, the resulting opacity may lower visual acuity. In our patients, however, we generally cannot demonstrate a reduction in vision in individuals having corneal dystrophy. The dog is the most common nonhuman species affected; the condition is rare in other species.

The subject of corneal dystrophy can be extremely complex. However, the practitioner needs to know which conditions constitute problems and which can be left alone. With this in mind, I suggest that these diseases can be understood by thinking in terms of which lead to problems for the patient and which are innocuous. The following is a breakdown of what to look for based on our present understanding.

Corneal dystrophies causing problems for the patient

There are no explicit guidelines to use in classifying these because two individuals may have a similar form of dystrophy and only one may be bothered by it. Thus, if the patient is bothered by a particular condition, it should be considered a problem.

Problem dystrophies affecting the anterior part of the cornea: The collie and Shetland sheepdog sometimes are affected by a multifocal dystrophy which is associated with irritation . The lesions appear as multiple, tiny, circular white (crystalline) superficial deposits in the anterior stroma. There may be subsequent vascularization; because the deposits seem to appear first, some people still consider this syndrome a dystrophy.

When the lesions are troublesome for the patient, topical steroids usually will help; use as needed.

The Manx cat may develop an anterior stromal edema which progresses to a marked epithelial edema with bullous keratopathy (Bistner, et al.). Eventually the epithelium and anterior stroma breakdown; the affected individual experiences considerable discomfort at this time. No therapy is beneficial. Contact lenses or osmotic agents could be tried.

Problem dystrophies affecting the posterior part of the cornea: The Boston terrier and Chihuahua may develop an endothelial dystrophy . The endothelial cells become dysfunctional leading to severe, relentless corneal edema. The lesion may begin in the center of one cornea and spread peripherally; the second cornea may become involved simultaneously or weeks to months later. Eventually, the corneal epithelium becomes affected by the chronic stromal edema and starts to form tiny bullae. These bullae rupture and heal and are associated with considerable pain. In the late stages, vascularization of the cornea may occur.

There is no effective therapy. Topical osmotic agents or a contact lens may help. The prognosis must be considered extremely poor. Topical steroids early in the disease may slow the progression.

Corneal dystrophies not causing problems for the patient

As with the problem cases, there are no specific guidelines.

Non-problem dystrophies affecting the anterior part of the cornea: The poodle and various other canine breeds may get localized crystalline deposits in the anterior corneal stroma (Waring, et al.). These deposits usually are central or paracentral; they rarely progress (get larger or more extensive) beyond a very limited extent.

Non-problem dystrophies affecting the posterior part of the cornea: Many Siberian huskies develop central, annular deposits of crystalline material in the posterior layers of the cornea (anterior to Descemet's membrane) (MacMillan, et al.; Waring, et al.). As the individual gets older, the originally clear center of the annulus begins to opacify; by the time the individual is very old, the entire central part of the cornea may appear opaque. Although this condition is not painful and the affected individuals do not demonstrate any untoward reactions, some opacities may become dense enough, when combined with dense nuclear sclerosis, to reduce vision.

Control

Individuals with corneal dystrophy should not be used for breeding.

Corneal degeneration

In many chronic corneal diseases accompanied by inflammation, there may be degeneration of the cornea. This may be manifest by the deposition of lipoidal material, particularly cholesterol, or calcium. There also may be bullous keratopathy where the epithelium or stroma develops vesicular changes; the vesicles may rupture and reform repeatedly. In some cases there may be loss of corneal tissue.

Corneal degenerations are secondary disturbances and should be differentiated from the primary corneal dystrophies. In most degenerations, there will be a history of ulceration, inflammation or other chronic problem; the cornea will be vascularized. These changes precede the deposition of metabolites. From a practical standpoint, if a particular corneal deposit is not causing trouble, it may be moot whether it is classified a degeneration or dystrophy. From a breeder's standpoint, however, it may be critical to know the difference.

Treatment of corneal degenerations depends on the cause and the stage of disease. If the lesion is inactive, no therapy is necessary. If the lesion is active, remove the cause and treat the cornea with topical medication (no steroids if ulcer present) until there is resolution of the inflammation; remember that most changes such as scarring or deposits will not disappear completely even after the original problem has been corrected.

Corneal lacerations

Although these are common, the toughness of the cornea prevents perforation in most cases.

Causes: Cat scratches are a common cause especially when pups encounter their first cat; these need vigorous therapy as will be described later. Fights, car accidents, contact with pointed objects and various other situations may lead to corneal laceration.

When there is a severe laceration, lack of a pupillary response in the opposite eye when the affected eye is stimulated with strong light may indicate severe posterior segment disease such as retinal separation (detachment) or dense vitreous hemorrhage.

Treatment:

Superficial wounds without excessive gaping of the edges: These heal rapidly, but should be treated with a topical antibiotic solution four times a day to prevent bacterial growth in the exposed stroma.

Deep wounds with gaping of the edges or production of a flap of cornea: If the wound is fresh and the edges can be apposed, use 6-0 or smaller absorbable or non-absorbable suture in a simple interrupted pattern. Treat as an uncomplicated ulcer. Non-absorbable sutures should be removed in 10-14 days.

If there is too much corneal damage to appose wound edges, treat it as a deep corneal ulcer as previously described.

Punctures without iris prolapse: These usually are sealed by fibrin-rich secondary aqueous and may require fluorescein dye for demarcation of the wound. These eyes usually are soft, painful and have a pinpoint pupil and aqueous flare.

These should be treated with a combination of systemic and topical antibiotics, a topical iridocycloplegic and cautious use of a topical corticosteroid.

Lacerations or punctures with prolapse of the iris: These are emergencies which require surgical intervention. The patient should be referred to a specialist immediately. The eye should not be manipulated.

If you cannot refer the patient to a specialist, you may have to attempt repair yourself. If the wound is less than a few hours old and if the iris is in good condition, the prolapsed portion may be reposited into the anterior chamber after careful flushing of the region with sterile balanced salt solution. If the wound is older and the iris prolapse is not extensive, the iris should be pulled gently from the wound so that fresh iris is exposed. The prolapsed portion of the iris is excised with a cautery blade or scissors (sharp excision may result in profuse bleeding, but soon will clot; blood in the anterior chamber usually spontaneously clears without trouble). The base of the iris plug should then return to the anterior chamber. The corneal wound is sutured using 6-0 or smaller absorbable or non-absorbable suture in a simple interrupted pattern. Because the cornea is dense and tough, only ophthalmic needles of the cutting type are satisfactory for suturing.

The sutures should be placed 1/2 to 2/3 the thickness of the cornea . Full thickness penetration can lead to leakage of aqueous humor which may prevent healing or lead to intraocular infection. It also can lead to epithelial downgrowth wherein corneal epithelial cells may grow down the suture wound and into the anterior chamber; this can be disastrous for the eye.

Medical therapy should be as in the case of a puncture without iris prolapse. Non-absorbable sutures should be removed in 10-14 days.

If there is a large amount of necrotic iris or unidentifiable uveal tissue protruding through the corneal wound and stimulation of the eye with strong light does not result in a pupillary response in the opposite eye, it is unlikely the eye ever will be functional. These eyes usually undergo phthisis bulbi and are best enucleated rather than repaired. This is mandatory in cats!

Prognosis: For small, recent iris prolapses and non-perforating wounds, scarring of the cornea and minor cataract formation may be all that occur leaving the eye essentially functional.

Eyes with extensive iris prolapse or eyes with severe postoperative inflammation usually develop extensive cataract or corneal scar formation and sometimes phthisis bulbi or glaucoma. The glaucoma in these cases usually is due to angle (ciliary cleft) closure secondary to inflammation and is refractory to therapy.

Cat scratches in dogs and others

This lesion is described separately because of its greater potential for severe consequences. The cat's claw often perforates the cornea and contaminates the anterior chamber. However, the wound is small in diameter and quickly seals; by the time the patient is brought to you, there may be re-epithelialization so that there is no fluorescein staining. The patient usually is comfortable and the eye appears quiet. Do not be misled by the benign appearance! Many of these develop a fulminating endophthalmitis in 3-4 or more days due to growth of inoculated bacteria. This often leads to glaucoma and eventual loss of the eye.

Regardless of how benign the injury appears, all patients having cat scratch trauma must be treated vigorously, both with topical and systemic antibiotics. An iridocycloplegic such as atropine should be used topically. Topical corticosteroids also are indicated unless the wound is a large laceration and retains fluorescein.

Corneal foreign bodies

Non-penetrating: This is foreign material which is adherent to the surface of the cornea, but has not entered the tissue. Small seeds or plant fragments are seen most commonly. Burdock pappus bristles, for example, are an important cause of keratitis in some regions (Pickett, et al.; Rebhun, et al.); they lodge in the conjunctiva and rub the cornea.

Affected individuals often will have blepharospasm and epiphora; the client may see the foreign body. If the condition has been present for several weeks, there may be some epithelial changes or minor vascularization. You may need magnification to see the offending particle.

The foreign body may be dislodged with a stream of saline from a syringe with a blunted cannula; use a topical anesthetic; use forceps to remove the dislodged object from the cul-de-sac. If this is unsuccessful, you will have to use forceps and, perhaps, a probe (simply a 22-25 gauge disposable needle); in this case, you should use general anesthesia to minimize the chance of causing further damage.

Medical therapy following removal of the foreign body in either case consists of topical antibiotic-steroid drops for several days.

Penetrating: Foreign bodies usually found include wooden splinters, thorns or plant fibers .

Affected individuals usually have sudden onset of pain and ocular discharge; a pertinent history may or may not be available. If uncomplicated, you may see the foreign body in a zone of corneal edema. If the anterior chamber has been entered and there is iris damage with hyphema, the foreign body may not be visible.

For treatment, general anesthesia is required. The eye should be prepared for intraocular surgery. If the foreign body protrudes from the corneal surface, you may be able to remove it with forceps. However, if it is flush with or beneath the corneal surface, do not use forceps because you may push the object deeper into the eye. Instead, use a probe (22-25 gauge needle) to go alongside and then under the object to pry it out; you may first have to make an incision in the cornea, parallel to the foreign body. If the cornea is perforated, suture it closed as described in previous sections.

After surgery these should be treated medically with systemic and topical antibiotics. Steroids are necessary, but should be avoided for a few days if the corneal wound is large. An iridocycloplegic is necessary.

If a foreign body is not visible, but you suspect one, treat as a uveitis. When clearing begins, you can re-examine to see if there is a foreign body. Once the eye becomes quiet, intraocular surgery may be required to extract the object.

Chemical burns

These are unusual in domestic animals, but when they occur, proper management will prevent serious damage. In humans, this is somewhat more common because of willful application of caustic agents such as lye.

For the sake of simplicity, the types of corneal chemical burns may be divided into those caused by alkalis or acids.

Alkalis

These are the most serious agents because topical alkali results in immediate death of the corneal (and conjunctival) cells and some denaturation of the stromal collagen. Collagenase production by regenerating epithelial cells, invading leukocytes, etc., then is responsible for causing progressive destruction with eventual perforation.

The initial treatment of these includes copious and continual flushing of the eye with saline. Human patients are hospitalized, a subpalpebral tube placed and a continuous flow of fluid is begun; this may be continued for as long as 24-36 hours.

Specific treatment includes frequent antibiotic and anti-collagenase drops. These must be continued for several weeks.

Corticosteroids are absolutely contraindicated in alkali burns because they potentiate collagenase activity.

Acids

These usually are not as serious as alkali burns because their initial effect is to precipitate protein which then prevents further penetration by the agent. Treatment would include moderate flushing of the eye with saline followed by frequent application of antibiotic drops until healing occurs.

Acquired corneal inclusion cysts

These are uncommon and are similar in appearance to those of congenital origin. Treatment is surgical excision.

Although not known, the suspected cause is trauma (Koch, et al.), especially of surgical nature; the theory is that epithelial cells may be introduced into the corneal stroma and begin growing.

Neoplasia

Primary neoplasms of the cornea are almost unknown. Most neoplasms of the cornea arise from adjacent conjunctiva. See section on conjunctival neoplasms for general comments, types, and treatments.