Technique

Ocular ultrasonography is performed directly through the cornea or the eyelids or by using an offset device. The optimal transducer for ocular ultrasonography is a 10- to 20-MHz probe, but one can use a 5- to 7.5-MHz probe. Ultrasound biomicroscopy (UBM) can be performed using 25- to-100 MHz probes, allowing detailed imaging of the cornea, limbus, iridocorneal angle, and anterior uvea. Sedation, auriculopalpebral nerve block, and topical anesthesia generally are required. Sterile, water-soluble lubricating jelly works well as a contact material, provided one irrigates the cornea afterward.

Normal Anatomy

With use of a 5- to 7.5-MHz probe, the cornea and a portion of the anterior chamber are lost in the near artifact unless an offset device is used. With a probe of 10 MHz or higher, the anterior chamber and cornea can be visualized. The anterior and posterior lens capsules are visible as an echodense line at the 12 and 6 o’clock positions, whereas the remainder of the normal lens is anechoic. The iris, corpora nigra, and ciliary body are often visible. The vitreous body is normally anechoic. The posterior eye wall is visible as a concave echodensity, with the optic nerve head visible as an echodense area at the posterior pole with an anechoic optic nerve posteriorly. The orbital contents are best visualized using a 7.5-MHz transducer to evaluate the extraocular muscle cone, optic nerve, and associated structures.

Indications

Ocular ultrasound is indicated for evaluation of intraocular contents when one or more of the ocular transmitting media are opaque, including opacification of the cornea, aqueous and vitreous humors, and the lens. The most common indications for ocular ultrasound are in eyes with a cataract to evaluate for a retinal detachment, after traumatic hyphema to assess posterior segment damage, or in eyes with severe corneal opacification. In addition, ocular ultrasound can be used to evaluate the orbit in instances of exophthalmos or orbital trauma. UBM can be used to determine depth of a corneal lesion such as a squamous cell carcinoma or to examine an anterior uveal mass for extent of involvement.

Congenital

Diseases of the equine eyelid are common. Congenital lesions include coloboma, agenesis, dermoid, and entropion.^3,4 Of these, entropion is the only frequently occurring disease. Entropion is inward rolling of the eyelid margin that results in facial hairs coming into contact with the cornea, leading to irritation, conjunctivitis, and possibly secondary corneal ulceration. Causes include prematurity or dehydration in foals with enophthalmos, ocular pain resulting in spastic entropion, and primary conformational problems. Manual reduction and frequent topical ocular lubrication with artificial tear ointment is the initial treatment of choice and may be the only treatment required in some foals, especially if the entropion follows dehydration. If the entropion is severe or does not respond to manipulation, the clinician may place two or three temporary vertical everting mattress sutures to position the eyelid correctly.³ It is important to avoid overcorrection, which could lead to the inability to close the eyelids during blinking. Suture placement is at and perpendicular to the eyelid margin, tacking this to the periocular skin over the orbital rim. Monofilament, 3–0 to 5–0 nylon suture is preferrable; the sutures are removed after 10 to 14 days. The clinician must treat associated corneal disease to prevent secondary infection and subsequent scar formation. Entropion requiring more aggressive surgical intervention in the form of skin excision is rare. Severe or recurrent entropion is correctable by excising an elliptic portion of eyelid skin in the affected area and reapposing the skin edges (Hotz-Celsus procedure).

Acquired

Common acquired conditions involving the equine eyelid include trauma and neoplasia.

TRAUMA

Eyelid trauma includes contusions and lacerations.⁵ Commonly associated with eyelid trauma are corneal abrasions or lacerations; anterior uveitis; and, if the trauma involves the medial canthus, nasolacrimal system damage. Eyelid contusions often result in blepharoedema and hemorrhage. Although mild blepharoedema does not require therapy, recovery can be hastened by using systemic flunixin meglumine (Banamine, Schering Corp., Kenilworth, New Jersey), cold compresses in the acute phase, and warm compresses beginning the day after the injury. In additon to the aformentioned therapy, severe blepharoedema may also require a temporary tarsorraphy and elevation of the head to protect the tissues and resolve the swelling (Figure 17-1).

FIGURE 17-1 A, Severe blepharoedema associated with facial trauma. B, A temporary tarsorraphy was performed standing to prevent exposure and dessication of the cornea and conjunctiva.

Eyelid lacerations are more serious and usually require immediate therapy (Figure 17-2). The vascular supply to the eyelid is extensive, and many apparent avascular segments of eyelid recover after repair. If possible, primary wound closure is preferable. It is important to remove all debris from the wound before closure, disinfect the eyelid surface and adjacent tissues with a 1:25 to 1:50 dilution of povidone-iodine solution, avoid excessive tissue débridement, and under no circumstances amputate a pedicle of eyelid. Loss of eyelid margin, whether iatrogenic or the result of trauma, leads to severe, chronic corneal irritation; vascularization; ulceration; and fibrosis (Figure 17-3). In addition, reconstructing an eyelid margin from the adjacent skin after amputation of the normal eyelid margin is difficult.

FIGURE 17-2 Tramatic laceration of the inferior lateral eyelid margin.

FIGURE 17-3 Failure to repair a superior eyelid lacretaion has resulted in contracture of the pedicle and exposure of the cornea.

One should suture lacerated eyelids using a two-layer closure, ensuring accurate anatomic apposition of the wound edges and eyelid margin. Minor surgical repairs can be performed using sedation and local nerve blocks, but the horse may require general anesthesia if the injury is severe. First, suture the deeper, conjunctival layer using 5-0 to 6-0 absorbable suture in a horizontal mattress pattern beginning away from and working toward the eyelid margin, taking care to avoid penetrating the conjunctiva so that the suture does not come into contact with the cornea. The practitioner then closes the skin with 5–0 to 6–0 nonabsorbable monofilament suture. The eyelid margin is the most important part of wound closure and is closed first to ensure accurate apposition. The author prefers to use a cruciate suture pattern at the eyelid margin and a simple interrupted pattern for the remainder of the skin closure. Failure to perform a two-layer closure or achieve precise apposition of the eyelid margin may result in ulcerative keratitis or other secondary complications.⁶ Postoperative therapy includes administration of antibiotics for 5 to 7 days for systemic effect; tetanus toxoid; warm, moist compresses; and flunixin meglumine if inflammation and swelling are a problem. Topical medication is not required for eyelid injuries unless corneal or anterior segment damage accompanies the injury. The practitioner must evaluate eyelid function, and the eyelid must provide adequate protection to the cornea. If the blink response is impaired, the cornea should be protected with topical lubricants as often as possible. Advanced blepharoplastic techniques for repair of severe eyelid trauma with resulting loss of tissue are beyond the scope of this chapter but are discussed in detail elsewhere.³

NEOPLASIA

The most common neoplasms of the equine eyelid are sarcoid and squamous cell carcinoma. In addition, melanoma, mast cell tumor, lymphosarcoma, basal cell carcinoma, and papilloma can affect the eyelid (Figure 17-4). The differential diagnosis for eyelid neoplasms includes parasitic diseases such as ocular habronemiasis and other causes of granulomatous skin disease. Treatment of eyelid neoplasia depends on the location, size, tumor type, age and purpose of the horse, cost, surgical skill, and equipment available. Treatment modalities include surgical excision, radiation therapy, intralesional chemotherapy, hyperthermia, immunotherapy, cryosurgery, or a combination of these. The aim of therapy is to eliminate or halt progression of the tumor while maintaining eyelid function and preserving the eye and vision. Complete excision with primary closure is the optimal treatment but often cannot be achieved because of limitations on availability of tissue for reconstruction and the extensive and aggressive nature of many eyelid neoplasms. If the veterinarian cannot appose eyelid margins after tumor excision, more involved blepharoplastic techniques, such as advancement skin flaps, may be indicated (Figure 17-5).

FIGURE 17-4 A, Melanoma of the superior eyelid. B, An excisonal biopsy is performed, and the resulting defect cannot be closed by primary closure of the eyelid margins. C, An advancement graft is performed to reconstruct the superior eyelid.

FIGURE 17-5 Squamous cell carcinoma involving the medial canthus and inferior eyelid of a 19-year-old Appaloosa.

Squamous Cell Carcinoma

Squamous cell carcinoma (SCC) involving the eyelid is usually erosive and ulcerative.⁵ The medial canthus is the most common site of origin (see Figure 17-6). Invasion of adjacent soft and bony orbital tissue is possible if the disease is untreated. Treatment of ocular SCC is discussed in detail in the sections on conjunctiva and third eyelid.

FIGURE 17-6 Squamous cell carcinoma affecting the temporal conjunctiva, limbus, and cornea.

Sarcoid

Periocular sarcoid is the second most common eyelid neoplasm of the horse. The average age of an affected horse is 4 years, and smooth and warty sarcoids occur. Orbital invasion and bony involvement are possible. Surgical excision is associated with frequent recurrence and often is combined with cryosurgery, hyperthermia, chemotherapy, or irradiation to ensure complete tumor destruction. Of all treatment modalities, radiation is the most expensive and yields the best overall success.⁷

Intralesional immunotherapy with cell wall extracts of bacillus Calmette-Guérin (BCG) in oil has been used effectively in repeated injections 3 weeks apart. A total of four doses usually is required for complete tumor regression, with the overall response reported to be 69%, provided the injection was intralesional.⁷ Injection of cell wall extracts of BCG is associated with local inflammation and tumor necrosis. During this period of inflammation, the clinician must protect the globe to prevent corneal desiccation or ulceration. The use of live BCG organisms or whole killed organisms has been associated with anaphylactic reaction and death and is discouraged. Adverse systemic reactions to cell wall extracts of BCG are rare, but premedication with systemic corticosteroids is advised.

Intralesional chemotherapy with cisplatin in an oil-water emulsion has been reported to result in regression of equine sarcoid.⁸ A series of four injections, spaced 2 weeks apart, with a mean dose of cisplatin of 0.97 mg/cm³ of tumor mass resulted in tumor regression in all treated horses. In addition, 87% of horses treated for sarcoids were relapse free at a 1-year follow-up. A larger study of intralesional cisplatin reported a cure rate of 96.3% for sarcoids and 88% for SCC at 4 years after treatment. ⁹

Parasites

Common parasites of the equine conjunctiva include Thelazia lacrymalis, Habronema spp., and Onchocerca cervicalis.¹⁴ In a necropsy sample the prevalence of Thelazia organisms in the conjunctival sac of horses is highest in young animals, with 43% of 1- to 4-year-old horses being affected.¹⁵ In most instances infection is not associated with clinical signs, but chronic conjunctivitis, seromucoid discharge, and conjunctival nodules can occur.³ The adult parasite may be visible on ophthalmic examination of the cornea and conjunctival fornix, and larvae may be visible on examination of centrifuged samples of nasolacrimal washes. Treatment includes removal of the adult worms, irrigation of the nasolacrimal system, topical corticosteroids to reduce inflammation, and fly control. The topical organophosphates echothiophate, 0.03% to 0.06% every 12 hours, or isoflurophate, 0.025% every 24 hours for 7 days, have been reported to kill the parasite.¹⁶ Systemic treatment with fenbendazole at 10 mg/kg orally every 24 hours for 5 days also is reported to be effective against Thelazia organisms.¹⁷

Ocular manifestations of equine cutaneous habronemiasis result when the house or stable fly deposits the larvae of the Habronema spp. on or around the eye.^3,18,19 The resulting granuloma is associated with inflammation, intense pruritus, and epiphora. Yellow, caseous granules are notable throughout the granulation tissue. Histologically, eosinophils and mast cells predominate. Diagnosis is based on clinical signs, location, season of the year, and histologic findings. Clinical appearance can simulate squamous cell carcinoma. Histologically, the differential diagnosis is equine cutaneous mastocytosis.^3,19 Ocular lesions are most common at the medial canthus and may involve the skin, nasolacrimal duct, third eyelid, or conjunctiva. Treatment of equine cutaneous habronemiasis varies, and no single treatment is routinely successful.¹⁸ Surgical excision, cryosurgery, local and systemic corticosteroid therapy, systemic ivermectin (single dose, 0.2 mg/kg intramuscularly), various larvicidal treatments in the form of topical and systemic organophosphates, and various topical formulations containing ronnel or metrifonate with a dimethyl sulfoxide vehicle are used^3,18,19 (Table 17-1). Dimethyl sulfoxide serves as a vehicle and has anti-inflammatory effects, possibly related to its ability to detoxify hydroxyl radicals generated by neutrophils. The aim of therapy is to kill the larvae while controlling the resulting inflammation. In addition, fly control is an essential part of an overall management program.

TABLE 17-1 Topical Preparations Used to Treat Equine Cutaneous Habronemiasis

The blood-sucking midge Culicoides nubeculosus transmits O. cervicalis microfilariae. After transmission the immature microfilariae migrate through lymphatics and can travel to ocular and adnexal tissues. The prevalence of equine onchocerciasis increases with age, with an overall prevalence of 50% to 60%.^14,20–22 The prevalence of onchocerciasis on histologic examination of the lateral bulbar conjunctiva is 10.8%. The presence of conjunctival microfilaria does not correlate with clinical abnormalities. Ocular onchocerciasis has been proposed as a cause of keratitis, conjunctivitis, equine recurrent uveitis, and depigmentation of the temporal bulbar conjunctiva.²² The pathogenesis is thought to involve the death of the microfilariae, release of antigens, and development of hypersensitivity in susceptible horses. Treatment is indicated in those horses with active conjunctivitis, keratitis, or uveitis attributable to onchocerciasis and includes anti-inflammatory agents such as topical corticosteroids and systemic flunixin meglumine; topical echothiophate iodide 0.025%; and systemic diethylcarbamazine, levamisole, or ivermectin³ (Table 17-2).

TABLE 17-2 Systemic Treatment of Ocular Onchocerciasis

Neoplasia

Neoplasms affecting the conjunctiva and third eyelid include SCC, lymphosarcoma, melanocytoma, mastocytoma, hemangioma, and angiosarcoma.^3,16 Diagnosis and characterization of adnexal neoplasms are based on history, signalment, location, appearance, and histopathologic examination. Routine surgical biopsy is performed with sedation, local nerve blocks, and topical anesthesia. Most adnexal neoplasms are benign or locally invasive, the exception being ocular angiosarcoma, which is reported to have a high incidence of metastasis.²³ Treatment of adnexal neoplasms varies according to tumor type, location, and size; use of the animal; treatment modalities available; and cost. The aim of treatment is to eliminate the tumor, restore normal anatomy, and maintain function of the eye and associated structures.

SCC is the most common tumor of the equine eye and adnexa (Figure 17-6). Involvement can be unilateral or bilateral, with the third eyelid and medial canthus affected most frequently.^16,24 Involvement of the corneal limbus, sclera, conjunctiva, and other adnexal structures also has been reported.^16,24,25

The mean age of onset for SCC is 9.8 years for all horses compared with 3.8 years for ocular sarcoidosis.²⁵ The incidence of ocular SCC is higher in draft-breed horses and Appaloosas than in light horses,^26,27 and sexually intact males and females have a decreased incidence.²⁶ Adnexal hypopigmentation and increased exposure to actinic radiation^25,26 are hypothesized to predispose horses to develop ocular SCC.

Ocular SCC is malignant and locally invasive with the potential to metastasize.^22,28 Metastases to local and cranial mediastinal lymph nodes, parotid salivary glands, and the thoracic cavity occur in 10% to 15% of patients.²⁷

Treatment of ocular SCC varies and must be designed for the individual patient. Surgical excision,²⁵ radiofrequency hyperthermia,²⁹ cryotherapy,³⁰ immunotherapy,³⁰ radiation therapy,^25,28–30 intralesional chemotherapy,^8,31 laser surgery,⁵ or a combination of these^29,30 have been used with success. Location, size, and depth of the tumor; visual status; financial commitment; purpose of the animal; and the presence or absence of metastatic disease influence the choice of therapy.

If possible, complete surgical excision is curative and is the preferred therapy. Difficulty arises with surgical excision when preservation of the globe and ocular and adnexal anatomy and function are required. Complete excision of the third eyelid is possible and often can be performed using sedation and local nerve blocks. To prevent possible herniation of the orbital fat, the clinician should appose the bulbar and palpebral margins of the third eyelid conjunctiva after excision using 5–0 to 6–0 absorbable suture in a simple continuous pattern.

Most SCCs are radiosensitive and can be treated successfully with sources of β- or γ-radiation. The major disadvantage of less expensive modes of radiation therapy, such as strontium 90 (⁹⁰Sr), a source of β-radiation, is the size limit of tumor amenable to treatment. With ⁹⁰Sr, for example, half the β-radiation produced is lost after passage through 1 mm of soft tissue. Thus the practitioner should limit treatment to lesions less than 2 mm deep, such as corneal, scleral, or superficial conjunctival SCCs. Radiation is most appropriate as an adjunct therapy after surgical removal of a corneal or conjunctival SCC. When used appropriately, ⁹⁰Sr can achieve a nonrecurrence rate for SCC of 87.5% after 2 years.³²

The use of interstitial radiotherapy for periocular SCC has been reported.^29,32 Radioactive gold seeds (¹⁹⁸Au) were used to impart a medium-energy γ-ray (0.41 MeV) with a half-life of 93.3 hours for a total recommended dose of 5000 rad.²⁹ Success rates of 80% at 1 year and 70% at 2 years are reported.³² Disadvantages of radioactive implants are their substantial cost, their limited availability, the risks associated with human exposure, and the licensing restrictions on their handling.²⁹ Secondary complications of interstitial radiation therapy include temporary corneal opacity, local necrosis, hair loss, damage to normal structures, and local depigmentation.^29,32 Although no retinal or lens changes have been reported after interstitial radiation treatment, the practitioner should consider the possibility of photoreceptor damage and cataractogenesis following radiation therapy.

Radiofrequency hyperthermia involves the passage of a radiofrequency (2 MHz) electric current between two electrodes. Tissue between these probes offers resistance, resulting in thermal energy being transferred to the tissue. Tissue temperature increases to 50° C in a 1-cm² area,²⁹ with malignant cells exhibiting a greater sensitivity to thermal energy than normal cells. The practitioner should not use topical radiofrequency hyperthermia as the only mode of treatment for tumors extending deeper than 3 mm or those greater than 4 to 5 cm in diameter. Superficial eyelid SCCs or corneal and conjunctival SCCs are most appropriate for treatment using radiofrequency hyperthermia. The practitioner should be careful not to overlap the fields of exposure, especially in corneal tumors, because this creates a risk of excessive necrosis of normal tissue.³³

Cryosurgery using nitrous oxide (–80° C) or liquid nitrogen (–185° C) in a single freeze- or double freeze-thaw cycle results in tissue destruction. Cryodestruction is most often indicated for treatment of eyelid SCCs. Associated local depigmentation of skin and hair may occur in the treated area. The practitioner should use thermocouples, and tissue temperatures of –25° C are optimal.

Intralesional chemotherapy with cisplatin or bleomycin in an oil-water emulsion has been reported to result in regression of equine SCC. Treatment is the same as previously described for eyelid sarcoidosis. Of those horses with adnexal SCC treated with intralesional cisplatin, 65% to 93% were relapse free at 1 year.^8,31 A second study reported a success of 88% at 4 years.⁹

Regardless of the treatment used, frequent and continued follow-up examinations result in the greatest long-term success in managing ocular and periocular SCC. Recurrence may happen at the initial site of involvement and must be distinguished from granulation tissue associated with the previous treatment. In addition, the practitioner must monitor other sites and the opposite eye for the development of new SCC lesions.

Anatomy and Physiology

The cornea consists of the epithelium, stroma, Descemet’s membrane, and endothelium. The epithelium is 7 to 15 cells thick and is replaced every 7 to 10 days. The corneal endothelium is a monolayer of cells with little to no regenerative capacity. Damage to the endothelium is therefore of great significance, because complete repair is often not possible and results in permanent corneal edema. The cornea is transparent and avascular and is supplied with sensory nerves from the ophthalmic branch of the trigeminal nerve. The epithelium and anterior stroma are innervated richly with sensory nerves, whereas the middle and inner cornea is less well supplied. Nutrition and waste removal are carried out by the tear film, aqueous humor, and diffusion to and from the scleral and conjunctival blood vessels. The cornea is maintained in a state of deturgescence by the mechanical barrier and pump mechanisms of the epithelium and endothelium. Interference with these barriers results in corneal edema, with endothelial damage being the more significant. Chronic irritation of the cornea results in superficial vascularization, whereas inflammation of the anterior uvea results in deep corneal vascularization. Corneal pigmentation often follows vascularization. Cellular infiltration of the cornea occurs in neoplastic, infectious, and inflammatory disease. All of these processes can occur alone or in combination, resulting in an alteration of corneal transparency. In addition, scar formation and noncellular infiltrates such as mineral and phospholipid deposits (corneal degeneration) alter corneal transparency. Establishing the cause of these changes and, if possible, eliminating the cause are essential.

Ulcerative Diseases

Corneal ulceration is perhaps the most frustrating and potentially devastating disease of the equine eye. Of all species commonly treated in veterinary ophthalmology, the cornea of the horse is the slowest to heal, is the most likely to become infected, and has the poorest prognosis for outcome. In addition, the size and temperament of the animal make frequent treatment difficult for owner and veterinarian. In most instances corneal ulceration results from an initial trauma, but secondary infection is common, especially in eyes treated with topical corticosteroids after ulceration.

CLINICAL SIGNS AND DIAGNOSIS

A corneal ulcer is a break in the corneal epithelium. Clinically, ulceration results in lacrimation, blepharospasm, photophobia, conjunctival hyperemia, corneal edema, and possibly miosis and aqueous flare. The diagnosis of a corneal ulcer is based on these clinical signs and fluorescein staining of the cornea. The underlying stroma retains the fluorescein stain and appears green. Before instilling any therapeutic or diagnostic agents in the eye, the veterinarian should submit bacterial and fungal culture samples from all corneal ulcers in the horse and should obtain culture samples from the margin of the ulcer. After obtaining culture samples and staining the cornea with fluorescein, the veterinarian applies topical anesthetic and obtains a scraping from the ulcer for cytologic examination. The cells are placed on a glass slide and stained to allow examination for bacteria, fungal hyphae, and cell type. Gram and Giemsa stains work well for examination. The presence of gram negative rods indicates the possibility of an infection with Pseudomonas spp., whereas cocci are suggestive of Streptococcus spp., a frequent and severe corneal pathogen. The presence of fungal hyphae is pathognomonic for mycotic keratitis, with Aspergillus spp. and Fusarium spp. being the most frequent corneal pathogens. Mixed bacterial and fungal infections are common.

A corneal ulcer is characterized according to size, depth, and the presence or absence of cellular infiltration. In addition, the veterinarian examines the anterior chamber for anterior uveitis. With all corneal ulcers, attempting to establish the cause of the ulceration and eliminate it is esssential (Figure 17-7). The veterinarian examines the palpebral conjunctiva and bulbar surface of the nictitans for the presence of a foreign body, evaluates the blink response and tear film, and obtains a complete history regarding trauma and previous medication. Topical corticosteroids should not be administered in the presence of a corneal ulcer, and a history of previous topical corticosteroid therapy increases the likelihood of infectious, especially fungal, keratitis.

FIGURE 17-7 A, Chronic, superficial corneal ulcer. The shape and orientation of the corneal ulcer suggest a foreign body on the bulbar surface of the nictitans. B, Foreign body removed after examination of the bulbar surface of the nictitans.

Some specific types of corneal ulcers in the horse include indolent ulcers,³⁶ ulcers with eosinophilic cellular infiltrate,³⁷ collagenase and mycotic ulcers, and possibly viral ulcerative keratitis.^3,16

ROUTINE TREATMENT

Treatment of an uncomplicated corneal ulcer involves controlling pain and inflammation, eliminating or preventing infection, and preventing secondary complications (Table 17-3). Healing occurs by migration and mitosis of the adjacent epithelial cells and, depending on the size of the ulcer, should be complete in 2 to 6 days for an uncomplicated corneal ulcer. Complicated corneal ulcers are those that fail to heal in an appropriate time, are secondarily infected, have an ongoing source of irritation or reulceration, have a collagenase component, are associated with corneal vascularization, or are worsening despite appropriate treatment.

TABLE 17-3 Commonly Used Ophthalmic Medications

If miosis is evident, the clinician can admininster topical atropine 1% to dilate the pupil, decrease the pain of anterior uveitis, and prevent posterior synechiae formation. Topical atropine is used as needed to dilate the pupil, but treatment frequency should not exceed 4 times daily. All topical ophthalmic medications are absorbed and have systemic effects, and topical atropine can result in colic following ileus. While administering topical atropine, the clinician should evaluate intestinal motility by auscultation, and the owner should observe for fresh fecal material in the stall every day. Systemic flunixin meglumine is indicated to suppress inflammation and control pain associated with a corneal ulcer, which in combination with topical atropine helps dilate the pupil.

Topical broad spectrum antibiotics such as neomycin-bacitracin-polymyxin B ophthalmic are the initial antibiotics of choice. Ointments are preferred for their ease of administration and prolonged corneal contact time. Frequency of administration varies according to severity of the disease. When topical antibiotics are used prophylactically for an uncomplicated corneal ulcer treatment, administration three or four times daily is sufficient, but in severe infectious keratitis, therapy might be hourly. If infection with Pseudomonas spp. is suspected, topical gentamicin, polymyxin B, tobramycin, or preferably ciprofloxacin or ofloxacin is indicated every 2 to 4 hours. Although gram positive organisms predominate initially in equine infectious keratitis, intensive topical antimicrobial therapy results in a significant shift to gram negative organisms and a change in susceptibility patterns.^38,39 Additional treatment varies according to the type and severity of the ulcer (see the section on complicated ulcerative diseases). Topical corticosteroids should not be administered to a horse with a corneal ulcer.

Complicated Ulcerative Diseases

Complicated corneal ulcers are those that require treatment over and above routine ulcer management, are infected, exhibit chronicity or recurrence, are in imminent danger of perforation, or have a collagenase component (Figure 17-8). Secondary infection of a corneal ulcer is suggested by increasing pain, corneal edema, interstitial keratitis associated with an increase in stromal inflammatory cells, corneal vascularization, purulent discharge, severe anterior uveitis, and stromal necrosis and liquefaction.

FIGURE 17-8 Deep corneal ulcer and descemetocele with associated focal corneal edema and miosis.

In many instances, complicated corneal ulcers require frequent and prolonged therapy, and some form of medication delivery system is indicated to ensure adequate treatment. Use of subpalpebral and nasolacrimal medication delivery systems has been described previously.⁴⁰ The author prefers to use the commercially available Mila lavage catheter (Mila International, Inc., Erlanger, ky.). When a lavage catheter is used, it should be kept clean and medication should be delivered to the eye slowly using air to push the medication through the tubing. Medication used with a subpalpebral lavage system must be in solution, not ointment. The volume of medication used at each treatment time should be 0.1 to 0.2 ml, and air must be used to deliver this medication to the eye. The use of irrigating solution to deliver the medication dilutes the medication. Once daily the system should be irrigated with sterile eyewash to ensure its patency and to rinse away mucus buildup.

Stay updated, free articles. Join our Telegram channel

Join