Revised from 6th edition of Veterinary Ophthalmology, Chapter 29: Equine Ophthalmology, by Caryn E. Plummer In order to perform a thorough examination of the equine eye, the patient must be adequately restrained. Chemical restraint greatly facilitates a complete ophthalmic examination of the horse. Typically, a short‐acting sedative is administered intravenously (i.v.), followed by an auriculopalpebral motor block. Xylazine (0.3–0.4 mg/kg i.v.) is usually adequate for examination. Especially difficult equine patients may require either a higher dose of xylazine (1.1 mg/kg i.v.) or detomidine (0.02–0.04 mg/kg i.v.) or romifidine (40–120 μg/kg i.v.). If more invasive diagnostic or treatment procedures are to be performed, such as corneal scrapings or conjunctival biopsies or placement of a subpalpebral (SPL) lavage system, most animals will require the more potent detomidine with or without the addition of butorphanol (0.01–0.02 mg/kg i.v.). The orbicularis oculi muscle closes the eyelids and, thus, can impair or even prevent ocular examination, especially in large animals. The pain in diseased eyes may be so intense that examining or manipulating the orbit and globe is difficult and potentially threatening to the integrity of the globe if the horse resists. The eyelids should never be forced open. A motor block to facilitate opening of the eyelids and visualization of the globe will target either the auriculopalpebral or palpebral nerves. These motor fibers may be blocked at three points between the origin of the auriculopalpebral nerve and the palpebral nerve branch: (i) just anterior to the base of the ear where the auriculopalpebral nerve emerges from the parotid salivary gland and becomes subcutaneous on the lateral aspect of the coronoid process. Here, a local anesthetic, such as lidocaine, may be injected into the depression just caudal to the ramus of the mandible at the ventral edge of the temporal portion of the zygomatic arch; (ii) just lateral to the highest point of the caudal zygomatic arch where the palpebral nerve can be “strummed” under the skin over the dorsal border of the bone; and (iii) where the palpebral nerve lies on the zygomatic arch caudal to the bony process of the frontal bone. Considering the branching of these motor fibers, more proximal blocks generally are preferred, because they affect more of the orbicularis oculi muscle. A 25‐gauge, 5/8‐in. needle is used to inject 1–3 ml of anesthetic subfascially adjacent to the nerve. In some instances, it is helpful to desensitize the skin of the eyelids to facilitate examination of the eye or to enable surgical repair of an eyelid wound or placement of a SPL lavage. Sensation to the eyelids is provided by the ophthalmic and maxillary divisions of the trigeminal nerve (i.e., cranial nerve V). In the horse, the frontal nerve innervates most of the central upper lid, the lacrimal nerve innervates the lateral upper lid, the zygomatic nerve innervates most of the lateral lower lid, and the infratrochlear nerve innervates the medial canthus. There are several different sensory blocks that may be employed in horses depending on the location of the eyelid lesion to be addressed. The central two‐thirds of the upper eyelid is innervated by the frontal or supraorbital nerve, and is blocked by injecting 2 ml of 2% lidocaine into the supraorbital foramen. This foramen can be identified as a small depression in the supraorbital process of the frontal bone, medial to its most narrow aspect (Figure 15.1). It can be palpated if the examiner places his or her thumb below the dorsal orbital rim and the middle finger in the supraorbital fossa. The examiner then places the index finger straight down midway between the thumb and middle finger to locate the supraorbital foramen. The lateral upper eyelid and lateral canthus are innervated by the lacrimal nerve, and can be blocked with a line block along the lateral third of the dorsal orbital rim. A block of the zygomatic nerve will anesthetize the lateral lower lid and is achieved with a line block along the ventrolateral orbital rim. The medial canthal region is innervated by the infratrochlear nerve and is desensitized by injecting anesthetic through the bony trochlear notch on the dorsal rim of the orbit near the medial canthus. Figure 15.1 Nerve blocks used in the equine eye exam. (a) The auriculopalpebral nerve block in a horse facilitates examination of the eye and is crucial when the cornea is fragile and near perforation. This figure illustrates the proximal placement of the block with the needle, while the arrows mark alternative locations that will elicit a similar response. (b) The injection of anesthetic agent. (c) The frontal (supraorbital) nerve is a branch of the trigeminal nerve and is blocked as it emerges from the supraorbital foramen within the frontal bone. (d) The supraorbital nerve block is performed at the level of the supraorbital foramen (directly within the foramen if possible, in the region if not) and is useful for anesthesia of the upper eyelid. To locate the supraorbital foramen, the examiner places his/her thumb under the orbital rim, the middle finger in the supraorbital fossa, and then places the index finger straight down midway between the thumb and middle finger to locate the supraorbital foramen. After preparation, the complete ophthalmic examination proceeds with a systematic approach. Following assessment of vision, and prior to instillation of any medication in or around the eye, the examiner should evaluate for symmetry of the head, bony orbits, eyelids, globes, and pupils in a well‐lit environment. The upper eyelashes of the healthy horse are nearly perpendicular to the cornea, while a ventral or downward direction of the eyelashes may indicate discomfort, enophthalmos, or ptosis. The menace response is assessed before sedation and motor blockade of the eyelids. Pupillary light and dazzle reflexes may be performed at any time. An assistant is helpful when assessing consensual pupillary light reflexes (PLRs). Then, the anterior and posterior segments of the globe are examined with a focal light source and magnification. Mydriasis is required for complete examination of the lens and ocular posterior segment. The most common mydriatic used is tropicamide (Mydriacyl® 1%, Alcon Laboratories, Fort Worth, TX, USA), which takes effect in approximately 10–20 min and lasts 4–6 h in the horse. If the horse has intraocular inflammation or anterior uveitis secondary to corneal disease or trauma, a single application of tropicamide may not fully dilate the pupil. Because of its longer duration of action, the use of atropine (1%) for routine examination is not recommended. Ocular disorders of the equine neonate may be congenital, inherited, or acquired. Normal embryogenesis of the foal eye results in fully developed globe and adnexa at birth. However, tear production and corneal sensitivity may be low initially, and lagophthalmos may be found in neonates. A menace response may not be fully developed until 10–14 days after birth. The PLRs, however, are intact, although may be sluggish initially. Hyaloid artery remnants in foals may contain blood for several hours after birth but generally disappear by three to four months of age. Lens sutures are often prominent in foals and should not be mistaken for a cataract. The anterior suture has a variable configuration in shape, with the posterior suture varying in shape from “Y,” sawhorse, to stellate patterns. Variations of the normal equine neonatal fundus are numerous, and primarily relate to coat color. The optic disc is oval to round, pink‐orange in color, and located slightly temporal in the inferior quadrant of the nontapetal fundus. The retinal vessels are small and extend only a short distance from the optic disc. No retinal vessels are found at the 6‐o’clock position of the horse optic disc. The foal tapetal fundus is usually blue to blue‐green, with small dots and end‐on views of choroidal capillaries or “stars of Winslow” distributed in a uniform pattern. Color‐dilute neonates may have light yellow zones of tapetal color with red “stars of Winslow,” or have no tapetum with resultant exposure of the choroidal vasculature, thereby creating a red fundic reflection. Light gray linear streaks arcing horizontally nasally and temporally away from the optic disc margin may be seen in the nontapetal fundus of foals, and represent axon bundles in the nerve fiber layer. Partial albinism will result in a lack of pigmentation in the retinal pigment epithelium (RPE) of the nontapetal region permitting visualization of the choroidal vasculature. An ophthalmic examination should be performed in foals 12–36 h after birth. Abnormalities are frequently noted on neonatal exams and these foals should be monitored regularly and carefully. Retinal and subconjunctival hemorrhages are common in neonates. Retinal hemorrhages usually resolve within one week, whereas subconjunctival hemorrhages may take several weeks to resolve. Ophthalmic lesions in neonatal foals with systemic disease are common; many including uveitis and ulcerative keratitis may be vision‐threatening. Foals with sepsis are significantly more likely to have anterior uveitis than were those without sepsis. Foals with sepsis and uveitis are also significantly less likely to survive than are foals that had sepsis without uveitis. Microphthalmos is a congenital globe condition in which the globe axial length is less than two standard deviations below the mean length (Figure 15.2). Thoroughbreds are at increased risk. Microphthalmos differs from phthisis bulbi, which is an initially normal‐sized globe that degenerates and atrophies secondary to severe injury or insult. Microphthalmos may be spontaneous and idiopathic, or it may be secondary to uterine infection or drug toxicity. Microphthalmos may be an isolated finding, or it may be associated with other ocular abnormalities, such as cataracts and retinal dysplasia. A small palpebral fissure and prominence of the nictitans are concurrent in affected foals. Entropion may occur from a lack of support from the small globe and be associated with mild‐to‐severe ulcerative keratitis. Corneal ulceration resulting from entropion and microphthalmia may necessitate entropion repair in visual globes or enucleation of nonvisual globes. Figure 15.2 Microphthalmos in a foal with nictitans protrusion and conjunctival exposure. The orbit is flattened on this side of the skull. Development of the bony equine orbit is influenced directly by globe development. Asymmetry of the face because of an underdeveloped bony orbit can be associated with congenital microphthalmos or phthisis bulbi resulting from early severe globe trauma in very young foals. Strabismus refers to a deviation in alignment of one globe in relation to the normal visual axis. When the two eyes fail to focus on the same image point, the brain may ignore the input from the deviated eye to result in a form of vision loss termed amblyopia. The two eyes may be crossed (esotropia), turned outward (exotropia), deviated up vertically (hypertropia) (Figure 15.3), or deviated down vertically (hypotropia). Foals with congenital or early onset strabismus do not receive the essential visual retinal stimulation for development of binocular vision and thus lack true stereopsis. Congenital strabismus and dorsomedial strabismus have been reported in Appaloosa foals with equine congenital stationary night blindness (CSNB). Hypertropia associated with congenital cataracts may resolve following surgical removal of the cataract. Dermoids (i.e., choristomas) of the eyelids, nictitans, cornea, and conjunctiva have been reported in foals (Figure 15.4). Corneal and conjunctival dermoids may appear as aberrant pigmentation when associated hair follicle development is minimal. Glands and follicles appear as hypopigmented foci on pigmented dermoids. Treatment depends on location. Superficial to deep keratectomy is indicated for corneal dermoids and excision with reconstructive blepharoplasty for eyelid dermoids is warranted to alleviate ocular irritation. Limbal dermoids have been noted with iridal hypoplasia and cataracts in Quarter Horses. Figure 15.3 Strabismus (hypertropia) in a foal with congenital cataract. Figure 15.4 Corneal dermoid in a foal. Note the pale spots within the pigmented lesion. Eyelid punctal atresia, nasolacrimal duct (NLD) agenesis, and nasal punctal atresia must be differentiated from acquired obstruction causing dacryocystitis of the nasolacrimal drainage system. NLD atresia, which is most commonly manifested by an imperforate nasal punctum, appears clinically as mild to moderate, unilateral or bilateral epiphora at 4–6 months of age and, if not managed appropriately, can develop into severe mucopurulent discharge by 10–12 months of age due to the development of secondary bacterial dacryocystitis. Culture and antibiotic sensitivity testing of the discharge and irrigated material are recommended. Contrast dacryocystorhinography (DCR) may be necessary to confirm the diagnosis. Eyelid punctal atresia may be noted visually at the medial canthus (lack of a punctal opening), because of distention of the conjunctiva over the atretic punctum after irrigation of the nasolacrimal system from the nasal punctum. A diagnosis of atresia of the nasal punctum may be presumed by noting the lack of a distal opening to the NLD within the mucocutaneous junction at the medial nares, failure of the irrigating solution to exit the nasal punctum during flushing of the proximal nasolacrimal system through the palpebral lacrimal punctum, and distention of the floor of the nasal vestibule in response to irrigation. Agenesis of the osseous NLD is fortunately rare but may also accompany the eyelid or nasal punctal atresia. Creation of a new proximal or distal opening and duct by catheter instillation is indicated for puncta atresia. It may be possible to flush the nasolacrimal system from the patent nares or canthal puncta to cause a dilation of the mucosa over the site of the atretic punctum. Once the atretic site is identified, an incision through the eyelid conjunctiva or nasal mucosa with a scalpel, cautery, or laser ablation will establish patency. To treat definitively, a #5 French male silastic or plastic urinary catheter is placed normograde from a proximal nasolacrimal punctum and pulled through the nares and sutured in place. The catheter should remain in place for several weeks (four to eight weeks) to allow epithelialization of the new duct and puncta and resolution of the dacryocystitis. Topical and systemic antibiotics are given for two to four weeks. Congenital corneal disease is uncommon in the horse, with megalocornea of multiple congenital ocular anomalies (MCOAs) of the Rocky Mountain Horse (RMH) and dermoids being most common. Aniridia, or complete absence of the iris, has been reported with congenital cataracts in Thoroughbreds, and as a sole lesion in Quarter Horses and Belgians. Aniridia, which is characterized clinically by the visualization of ciliary body processes and edge of the lens, has been reported to be inherited as an autosomal dominant trait in the Belgian Draft breed, the Quarter Horse, a Thoroughbred, and a Thoroughbred/Welsh cross. In spite of the terminology, total aniridia is rare and the base of the iris is usually present histologically in most cases. Discomfort from true photophobia and glare in conditions of bright light may be present due to the inability to regulate light entering the eye. Figure 15.5 Congenital iris abnormalities in foals. (a) Iris hypoplasia dorsally causes a cystic bulging of the dorsal iris stroma. (b) In this foal, the hypoplastic iris is so thin that the equator of the lens is visible behind the iris. Iris colobomas, both typical and atypical, may occur uncommonly in horses but should be differentiated from iris hypoplasia, which is an iris defect commonly observed in lightly pigmented irides (Figure 15.5a and b). Iridal hypoplasia is a congenital underdevelopment of the iris stroma that appears as thin iris tissue often with holes or defects. In iridal hypoplasia of heterochromic eyes, the affected thin region of iris stroma may appear dark due to the exposure of the posterior pigmented epithelium of the iris and it may appear cyst‐like if it balloons into the anterior chamber from the higher pressure of the posterior chamber. It is common in Appaloosas, Miniature Horses, and ponies and in blue and heterochromic eyes. Persistent pupillary membranes (PPMs) are remnants of the anterior tunica vasculosa lentis. They appear as strands of iridal tissue arising from the mid‐iris collarette and, in most cases, passing to attach to the iris, though attachment to the lens and/or cornea is possible. Nonprogressive corneal opacity results if the PPM adheres to the cornea, or a focal cataract can result if it adheres to the lens. These membranes generally regress to some extent over the first 6–12 months of life, and they require no treatment. Anterior segment dysgenesis (ASD) is characterized variably by observation of PPMs and may be a component of the MCOA syndrome of RMHs. ASD is associated with a missense mutation in the PMLE17 gene, often referred to as the silver dapple gene in the horse. Breeds affected include the Shetland pony, Miniature Horses, RMH, Kentucky Mountain Saddle Horse, Mountain Pleasure Horse, Morgan Horse, Bashkir‐Curly Horse, Narragansett Pacer, and Haflinger. Chocolate coat color and flaxen mane and tail color are often associated with the ASD (Figure 15.6a and b). Hypoplasia of the corpora nigra and iris, and temporal iris and ciliary body cysts are found in the heterozygous RMH. The homozygous state has congenital miosis with the pupil frequently nonresponsive to mydriatic drugs, deep anterior chamber, macrocornea, ciliary body and retinal cysts, cataract, lens luxation, RPE streaks, and retinal dysplasia/detachment. Hyaloid artery apparatus consists of the hyaloid artery and the posterior tunica vasculosa lentis. Remnants of some segment of this apparatus are apparent to some degree in both eyes of ~80% of Thoroughbred neonates less than four days old. It is perfused with blood in about a third of the eyes at birth, and becomes nonperfused by 48 h postpartum. These remnants appear as white linear opacities at the surface of the posterior lens capsule. Persistence of any part of the hyaloid artery system does not generally cause problems, although small posterior axial cataracts may be present in some eyes. Congenital defects of the lens may be due to genetic causes (inherited), toxins, nutritional imbalance, ionizing radiation, inflammation, or other idiopathic causes, although these causes have not been well characterized in horses. However, cataracts are the most common congenital abnormality in foals, representing approximately 35% of all congenital ocular defects (Figure 15.7a and b). Inherited congenital cataracts have been documented in Thoroughbreds, Quarter Horses, and Morgans. RMHs can also develop congenital cataracts, and lens luxation associated with ASD. A dominant mode of inheritance has been reported in Belgian as well as in Thoroughbred horses. Morgan horses have nonprogressive, nuclear, bilaterally symmetrical cataracts that do not seriously interfere with vision. Figure 15.6 Horses affected with MCOA. (a) Individuals with the silver dapple coat color (mutations at the PMEL locus) may be affected with ASD. Homozygotes tend to be more severely affected than heterozygotes. The chocolate coat color with a flaxen mane and tail is a silver dilute version of a black horse. (b) Temporal nonpigmented ciliary body cyst in a heterozygous RMH. Figure 15.7 Congenital cataracts in foals. (a) Remnants of the tunica vasculosa lentis remains perfused on the posterior lens capsule of this yearling. (b) Advanced immature cataract in a Thoroughbred foal. Healthy foals with cataracts, visual impairment, the personality to tolerate administration of topical therapy, and free of active anterior uveitis are candidates for cataract surgery. Preoperative ocular testing to establish candidacy for surgery proceeds as in small animals with electroretinography (ERG) and ocular ultrasonography. Foals should be carefully evaluated for any subclinical infectious systemic diseases, such as Rhodococcus pneumonia, because sight‐threatening postoperative endophthalmitis may result after surgery if the condition is not detected and treated preoperatively. The most common technique for removing congenital cataracts in foals is phacoemulsification. Recent advances in the surgical technique have increased the success rate in foals to nearly 80%. The logistics of general anesthesia and surgery as well as the surgical success rate are most favorable in foals less than six months of age. Postoperative iridocyclitis is generally quite minimal compared with that found in the dog; however, diligent medical therapy and monitoring is warranted. The visual outcome of cataract surgery can be difficult to evaluate in young horses. Foals left aphakic after cataract surgery are profoundly hyperopic, but in many cases have appropriate visual behavior. The placement of artificial intraocular lenses is advocated at present; however, the most ideal dioptric strength is still a matter of debate. Glaucoma is an elevation in intraocular pressure (IOP) that is detrimental to normal ocular function. The reference ranges for normal IOP in horses range from 17 to 28 mmHg. Elevation IOP that is incompatible with ocular health results from an obstructed outflow of aqueous humor, eventually resulting in optic nerve damage and blindness. Congenital glaucoma is generally associated with developmental anomalies of the iridocorneal angle. No particular breed predisposition has been reported for glaucoma in equine neonates. Glaucoma can also be a sequela to severe or untreated anterior uveitis in foals. Clinical signs of glaucoma include generalized corneal edema, narrowing or fibrosis of the iridocorneal angle, deep linear and branching corneal band opacities of Descemet’s membrane (DM), and the posterior stroma, lens luxations, optic nerve cupping, and a fixed, dilated pupil. Buphthalmia will occur if IOP is persistently elevated (Figure 15.8). Though glaucoma can be treated medically, surgical therapy may be best for foals with ASD. Surgical therapy for equine glaucoma is directed at reducing the production of aqueous humor by damaging the ciliary body with laser energy (i.e., cyclophotocoagulation). High‐flow gonioimplants may be considered to increase the aqueous outflow in foals. This is a difficult disease to manage in the foal, with little to no chance of preserving vision even if the condition is both detected and treated surgically early in its course. Chronically painful and blind, buphthalmic globes should be enucleated. Figure 15.8 Corneal edema from congenital glaucoma in a foal. Figure 15.9 Ocular fundus abnormalities in the foal. (a) Focal peripapillary RPE coloboma. This is a common congenital abnormality without known clinical significance. (b) Retinal dysplasia in a Thoroughbred foal. Fortunately, congenital abnormalities of the equine posterior segment are uncommon and rarely have clinical significance, such as the case with focal colobomas (Figure 15.9a). Other defects, such as congenital retinal detachment, retinal dysplasia, CSNB, and the MCOA syndrome (i.e., the RMH syndrome), may be associated with vision loss. Retinal dysplasia is an in utero developmental or postinflammatory problem of the retina in which the sensory retina is “folded” to form rosettes of neural tissue (Figure 15.9b). Retinal dysplasia in foals is generally bilateral and often associated with other congenital ocular problems. It can appear as either single or multiple, or linear or geographic foci or regions of hyporeflective folds or hyperreflective thinning on ophthalmoscopy. Retinal detachments may be either unilateral or bilateral, and they can be associated with other ocular abnormalities (Figure 15.10). The detached retina can be observed through the dilated pupil as a floating veil of opaque tissue in the vitreous. If the detachment is bilateral, the foal will be blind and may have nystagmus. CSNB has been reported in Appaloosas, Quarter Horses, Miniature Horses, Standardbreds, and Appaloosa horses with leopard complex spotting. It has also been reported in a Thoroughbred and a Paso Fino. The fundus appears to be structurally normal, with characteristic, a‐wave‐dominant ERG patterns confirming the diagnosis. A defect in neural transmission between the photoreceptor layers and the bipolar cells is suspected. Vision is severely diminished in reduced light levels, but functional in bright light. Figure 15.10 Congenital retinal detachment in a foal. The retina is torn and appears as a convoluted opaque membrane. Optic nerve hypoplasia and optic nerve atrophy in foals may be secondary to developmental or inflammatory processes. Foals with optic nerve hypoplasia display smaller‐than‐normal discs, have slow PLRs and mydriasis, and depending on the degree of hypoplasia may retain some vision. Foals with bilateral optic nerve atrophy are blind with fixed, dilated pupils, have pale discs with no retinal vessels, and have posterior depression of the optic disc of several diopters. Entropion is inversion of the margin of the lower or upper eyelids. It may occur in foals as a primary anatomical condition, or be secondary to the enophthalmos associated with microphthalmos or prematurity (Figure 15.11a and b). Rolling in of the eyelid margin may occur with dehydration or malnutrition in systemically compromised foals. It is the most common eyelid abnormality in foals and is most commonly exhibited in only the lower eyelid; however, it may affect the upper eyelid in Miniature Horses. Ocular pain may cause spastic entropion that may exacerbate the degree of anatomical entropion present. Treatment involves physical eversion of the eyelid margin with temporary, nonabsorbable sutures in a vertical mattress pattern (4‐0 silk) or with surgical staples until the underlying etiology has resolved or the foal has outgrown its entropion. Permanent reconstructive entropion surgeries should be reserved for full‐grown individuals. Figure 15.11 Eyelid abnormalities in foals. (a) Severe lower lid entropion and blepharitis in a foal. A corneal ulcer is present. Note the corneal edema and infiltrate ventrally. (b) The entropion was corrected with temporary tacking vertical mattress sutures. Ectropion is eversion of the lower or upper eyelid margins and generally follows scarring of the eyelids from severe trauma or burns. It is less common than entropion. Surgical correction is necessary for ectropion if blepharospasm, corneal ulcers, or exposure keratoconjunctivitis is present. Traumatic eyelid lacerations and forehead trauma can occur in foals and adults (Figure 15.12a and b). Upper eyelid lesions are more serious than lower eyelid injuries, because upper eyelid provides the greater degree of globe protection and its movements distribute tear film to prevent exposure keratitis. Thus, preserving the eyelid margins to prevent trichiasis and exposure‐induced ulcerative keratitis is critical. Excision of lacerated pedicles of eyelid marginal tissue should be avoided. The prominent blood supply to the eyelids generally allows acceptable and functional surgical repair, as well as faster healing. Two‐layer closure of skin–orbicularis muscle and tarsoconjunctival layers is recommended to maximize healing and return to function Dacryocystitis is inflammation of the tear drainage system. Obstruction of the nasolacrimal apparatus is the most common cause of dacryocystitis and secondary infection often develops. Copious mucoid to mucopurulent discharge at the medial canthus is the typical presenting sign. This condition is treated by flushing of the tear drainage system to reestablish patency and then administering systemic antibiotics and anti‐inflammatory medications. Topical steroids and mucolytic agents may be helpful if they are formulated as solutions or suspensions so that they can pass through the duct. Conjunctivitis caused by environmental irritants (e.g., hay, sand, dirt, ammonia, pollen, and ash) is common in neonates, with recumbent foals being at particular risk. Conjunctival inflammation associated with pneumonia or other systemic infectious and inflammatory conditions is often found in older foals (i.e., one to six months of age). Epiphora, chemosis, and hyperemia are typical clinical signs. If bacterial conjunctivitis is present, the ocular discharge will become mucopurulent. Conjunctival cytology and culture can be useful in making the diagnosis of infectious conjunctivitis. Therapy begins by flushing the conjunctival sacs to remove any underlying irritant. Patency of the NLD should be established, because duct obstructions can exacerbate conjunctivitis. Broad‐spectrum antibiotic ophthalmic solutions or eye lubricants are indicated, and corticosteroid ophthalmic preparations are useful if there are no corneal ulcers present. Figure 15.12 (a) Severe upper lid laceration in a horse. (b) Surgical repair of the laceration improved function and appearance. Subconjunctival or episcleral hemorrhages can result from birthing trauma and generally resolve in 7–10 days. No treatment is necessary. Traumatic hemorrhages are generally quite large and must be differentiated from the petechial or ecchymotic hemorrhages suggestive of a coagulation disorder. A corneal ulcer is present when there is a break in the corneal epithelium, most commonly caused by trauma or exposure. Foals, especially those under intensive care, should be monitored for the development of corneal ulcers. Foals with corneal ulcerations generally will exhibit less intense pain, blepharospasm, and tearing than their adult counterparts. This is likely due to immature sensory innervation. The corneal surface of superficial ulcers can appear dull, cloudy, and roughened. In rapidly progressive or infected ulcers, the corneal stroma may be “melting,” as the result of keratomalacia. Although many types of ulcers in foals are sterile, every corneal wound is susceptible to infection with bacterial and fungal pathogens (Figure 15.13a and b). Diagnostic testing to look for involvement of these agents should always be performed. A superficial corneal ulcer that does not improve rapidly in 24–48 h, rough ulcer margins, increasing stromal opacification, deepening of the ulcer, and difficulty maintaining mydriasis are often signs of ulcer infection. Medical therapy for foals with ulcerative keratitis does not differ substantially from that initiated for corneal ulcers in adults. Bacterial and fungal growth must be halted or prevented with antimicrobial agents. Anterior uveitis must be controlled for comfort and to prevent blinding sequelae. Anterior uveitis in foals with corneal ulcers should be treated with both topical atropine and systemic nonsteroidal anti‐inflammatory drugs (NSAIDs). A reduction in the tear film and stromal protease activity is also critical to healing of corneal ulcers in foals, particularly since they are prone to the development of melting ulcers. Melting ulcers in foals may be sterile (while those in adults are usually infected); however, they may progress rapidly and catastrophically if the enzymes responsible for corneal degradation are not arrested. The appearance of a gray, mucoid, gelatinous corneal exudate should prompt immediate action. Autogenous serum from the foal or its mare may also be quite effective in arresting corneal melting when administered topically every hour. Five percent acetylcysteine or 0.17% dipotassium ethylenediaminetetraacetic acid (EDTA) may be used as well until stromal liquefaction is reduced. Combinations of these anticollagenase drugs should also be considered if the ulcers are rapidly progressive. Surgery should be considered if the integrity of the cornea is compromised. Treatment must be sustained until the stroma has firmed and the epithelium has completely regenerated. Figure 15.13 Corneal ulcerations in foals. (a) Melting ulcer (keratomalacia) in a foal. The dark focus is a very thin in the center of the wound. (b) Fluorescein retention delineates the borders of a corneal ulcer. Very slow‐healing, persistent, superficial corneal ulcers are commonly encountered in recumbent, premature, and neonatal foals. These ulcers or erosions often fail to vascularize and affected foals may not exhibit a great deal of discomfort. Diminished corneal sensitivity and low tear production in these foals may be associated with the delayed corneal healing of these superficial ulcers. If the foals are blinking poorly, or keratoconjunctivitis sicca (KCS) or entropion is present, corneal ulcers will also heal slowly. Therapy is directed at treating any underlying cause (such as tacking sutures from entropion), removing abnormal epithelium, and promoting adhesion of the epithelium to its basement membrane and the stroma. The cornea should be topically anesthetized and the loose abnormal epithelium gently debrided with dry, soft cotton swabs. Debridement may need to be repeated, or may require a more aggressive approach and the use of a diamond burr to minimize any suprastromal membrane that may be inhibiting epithelial migration and adhesion. Antibiotic solutions are indicated to prevent infection. The triple antibiotic solutions are appropriate, while solutions containing gentamicin should be avoided as they can retard corneal healing. Five percent sodium chloride ophthalmic preparations are beneficial in removing the superficial corneal edema associated with persistent ulcers and topical autogenous serum or plasma with its growth factors and anticollagenase activity can promote epithelial growth and prevent stromal melting from tear proteases. If healing stagnates despite debridement and medical therapy, a keratectomy may be indicated. Systemic disease can cause blinding iridocyclitis in foals; therefore, early recognition, diagnosis, and therapy are imperative. Septic foals or those with another systemic inflammatory disease such as pneumonia may be afflicted with anterior uveitis as a manifestation of their systemic disease. Salmonella sp., Rhodococcus equi, Escherichia coli, Streptococcus equi subspecies equi, Actinobacillus equuli, adenovirus, and equine viral arteritis have all been associated with uveitis in affected foals. Lacrimation and blepharospasm are usually the signals of ocular involvement and will accompany corneal edema, conjunctival hyperemia, ciliary injection, aqueous flare, hyphema, fibrin, and hypopyon in eyes with iridocyclitis. Miosis is evident initially as the hallmark of uveitis and it can result in dyscoria as well as in anterior and posterior synechiae. Fibrin and pigment deposition on the anterior lens capsule and cataract formation are sequelae to anterior uveitis in foals. As long as a corneal ulcer is absent, topical corticosteroids are the treatment of choice for anterior uveitis and these are usually accompanied by mydriatic/cycloplegics and systemic NSAIDs (as long as the systemic condition of the foal warrants their use). If a corneal ulcer is present, that would preclude use of topical corticosteroids but not topical NSAIDs. Many foals with systemic disease will develop fibrinous uveitis. Fibrin may fill the anterior chamber and span the pupil increasing the chances of synechia and cataract formation. If routine anti‐inflammatory therapy does not result in rapid degradation of the anterior chamber fibrin (48–72 h), intracameral administration of 25–150 μg tissue plasminogen activator (tPA) under heavy sedation or general anesthesia may be used to accelerate fibrinolysis and clear the anterior chamber of foals with severe iridocyclitis. tPA should be avoided if recent hemorrhage (<48 h) is present, but can still be effective up to two weeks after clot formation. Depending on the cause, the overall prognosis for anterior uveitis is guarded in foals, depending upon its severity and response to therapy. The owner should be educated about the possibility of phthisis bulbus, vision loss, and other potential complications. The orbits and globes of the horse skull are directed anteriorly, slightly dorsal, and are positioned 80° lateral to the midline to allow for wide panoramic vision. The orbits of the skull are bony cavities formed by the frontal, lacrimal, zygomatic, temporal, sphenoid, and palatine bones, and function to protect the globe. The orbits of the horse are open anteriorly, closed posteriorly, possess a soft tissue ventral floor, and contain osseous canals, fissures, and foramina. Sinuses surround the orbit. The anterior rim of the bony orbit is complete in the horse. This complete bony orbital rim anteriorly and bony orbital walls posteriorly is a factor in the horse sustaining comparatively more orbital fractures than in other domestic animals. Because of this bony protection and strong extraocular muscles, horses rarely develop orbital trauma, except penetrating injuries. The essential components of the orbital connective tissues are the periorbita, the orbital septum, and the episcleral fascia or Tenon’s capsule. The frontal sinus is located dorsal and ventral to the medial orbit. The maxillary sinus is located ventral and nasal to the orbit. The anterior maxillary sinus can be located just ventral to the intersection of a line between the medial canthus and infraorbital foramen, and a perpendicular line from the fourth cheek tooth. Trephination dorsal to a line between the infraorbital foramen and medial canthus can result in NLD damage. The center of a line between the medial canthus and facial crest indicates the location of the caudal maxillary sinus. The sphenopalatine sinus is located medial and ventral to the orbit. With the exception of the anterior maxillary sinus, all sinuses in the horse communicate with one another. Sinus disease (infection, neoplasia, and other clinical abnormalities) involving the frontal, maxillary, or sphenopalatine sinuses often intrudes upon the orbit of horses. The lacrimal gland, orbital fat, and connective tissue fascia completely fill the orbital spaces between the globe, extraocular muscles, optic and other cranial nerves, and orbital vascular elements of horses to provide a cushion that protects these delicate structures from injury during ocular movements. The lacrimal gland is situated dorsolaterally between the zygomatic process and the globe. It is separated from the globe by periorbital fascia, and opens via 12–16 small ducts along the lateral part of the conjunctival sac in a line anterior to the dorsal conjunctival fornix. A cushion of fat lies in the ventral equine orbit. Orbital disease can result in exophthalmos because of space‐occupying orbital lesions, or enophthalmos if the volume of the orbital contents decreases because of malnutrition, pathology, or surgery (Figure 15.14). Both the degree and direction of exophthalmos depend on the size and location of the lesion. Intraconal lesions cause anterior displacement of the globe, whereas lesions of the medial orbit displace the globe laterally. The nictitating membrane usually protrudes with exophthalmos, and if the exophthalmos is severe, exposure keratitis can then result because of inability of the lids to cover the cornea. Large space‐occupying masses, such as tumors, bone fragments, or hematomas, can limit globe motility and impair the ocular circulation. The size of the exophthalmic globe is normal and should not be confused with the globe enlargement (i.e., buphthalmos) with advanced equine glaucoma. Figure 15.14 Periorbital sinuses. The frontal (conchofrontal), maxillary (caudal and rostral), and sphenopalatine are in close anatomical proximity to the orbit. Making the diagnosis of orbital disease usually requires imaging techniques in addition to a complete ophthalmic examination. Commonly used diagnostic imaging tools include orbital ultrasound and skull radiographs. Ultrasonography allows visualization of the retrobulbar soft tissue space and differentiation between solid, soft tissue lesions and cystic orbital lesions; however, evaluation of the extent of disease is not possible with ultrasonography. The extensive overlap of the many bones of the skull makes interpretation of skull radiographs challenging. Although commonly used, the extent and severity of injury are not well characterized by these modalities. When possible, computed tomography (CT) is the imaging modality of choice in equine orbital disease, especially if there is concern for bone involvement. Magnetic resonance imaging is useful for characterizing soft tissue disease. Retrobulbar nerve blocks can facilitate ocular and orbital procedures performed standing or under general anesthesia required for enucleation surgery by minimizing the depth of the plane of anesthesia necessary. Retrobulbar blocks are standard of care for enucleation and exenteration procedures, and should be performed in all cases undergoing these surgeries. For the supraorbital technique, a 22‐gauge 3.5‐in. spinal needle is inserted through the surgically prepped skin of the supraorbital fossa just caudal to the posterior aspect of the dorsal orbital rim. The needle is advanced until it reaches the retrobulbar muscle cone. This can be detected by slight dorsal movement of the eye. Once positioned, 10–12 ml of an anesthetic agent (lidocaine, bupivacaine, or mepivacaine) is injected into the orbit. Slight exophthalmos and mydriasis will occur with a properly placed block. The four‐point block involves placing the needle through the conjunctival fornices and dividing the volume of the block among the quadrants (dorsal, ventral, medial, lateral). Enucleation is the surgical removal of the globe, conjunctiva, and nictitating membrane. There are two basic approaches to enucleation in the horse: the transpalpebral technique and the subconjunctival technique. The transpalpebral technique is most useful in cases of severe corneal infection and conjunctival, nictitating membrane or corneal neoplasia, but it does leave a larger orbital soft tissue defect than the subconjunctival technique. The subconjunctival approach is quicker and associated with less hemorrhage. Orbital silicone prosthetic implants to improve cosmesis (decrease orbital “pitting” or “sinkage”) may be used with either method. However, there is an increased risk of postsurgical infection when orbital prostheses are placed. Orbital exenteration is a surgical technique used to remove malignant tumors of the orbit that extend beyond the confines of the globe or are likely to be unresponsive to chemotherapy or radiation therapy. In this procedure, the entire orbital contents, including the periorbita, are surgically removed. Periosteal elevators may be needed to remove the periorbital fascia; the remaining tissue is excised using scalpel or scissors. The intraocular (sometimes referred to as intrascleral) prosthesis has been used in the horse as a cosmetic alternative to enucleation. The intrascleral prosthesis replaces the intraocular contents, which are removed by evisceration. Implants should not be placed in eyes with severe corneal disease, intraocular neoplasia, or infectious panophthalmitis. The prosthesis provides a cosmetically acceptable globe with normal lid movements and globe motility. Perforation by a foreign body, direct trauma, and seeding by septic emboli are among the more common causes of orbital cellulitis. Extension of inflammatory and infectious conditions from adjacent sinuses and cavities also occurs commonly. If sinusitis is present, trephination into the affected sinus for the culture of exudate as well as irrigation and drainage is indicated. If septic endophthalmitis is untreated or is poorly responsive to therapy, it may progress to panuveitis and orbital cellulitis. Orbital cellulitis is manifested by blepharedema, swelling of the supraorbital fossa, exophthalmos, orbital pain, epiphora or mucoid discharge, and protrusion of the nictitans, conjunctival hyperemia and chemosis, and sometimes lagophthalmos. Fever, elevated white blood count, and general malaise may also be present. Orbital ultrasonography, CT, and fine needle aspiration may be helpful in the diagnosis. Aggressive use of systemic NSAIDs and broad‐spectrum antibiotics is indicated. Rarely is there a discrete fluid pocket in the abscess, so attempts at drainage are usually not fruitful or effective. If there is no response to therapy and the globe is damaged, then enucleation or exenteration may be needed. Fractures of the orbital bones may present with asymmetry of the globes or face, epistaxis, exophthalmos, eyelid and conjunctival swelling, depression or concavity of the periorbital region, crepitus, and sometimes pain on periorbital palpation. Fractures of the dorsal orbital rim are most common (Figure 15.15a and b) because the dorsal orbital rim protrudes externally and laterally and is thus highly vulnerable to trauma. These fractures may result in displacement, impingement, functional restriction, or laceration of the globe. Figure 15.15 (a) Fractures of the dorsal orbital rim are most common in horses, likely because the dorsal orbital rim protrudes externally and laterally, and thus is highly vulnerable to trauma. (b) Fracture of the dorsal orbital rim of a horse that resulted in ventral deviation of the globe and ventral strabismus. Diagnosis and assessment of orbital rim fractures should be accomplished by a thorough ophthalmic examination and digital palpation. Imaging by radiography, and preferably CT, should be performed prior to considering surgical intervention. Skyline views are helpful for the orbital rim, but they can be difficult to interpret Periorbital fractures should be repaired quickly, because fibrous union of the fractured pieces begins within one week after injury making elevation and realignment difficult. Minor orbital rim fractures that are closed and nondisplaced may not require surgical correction unless fracture fragments are impinging on the globe. Any section of bone that is impinging on the globe or orbital contents needs to be reduced or removed. With the horse placed under general anesthesia, zygomatic process fractures may be reduced or closed by manipulation of the bone piece into position using a bone hook. Monofilament stainless steel wire suture (20–22 gauge), cerclage wire, small orthopedic pins, and orthopedic bone plates and cancellous bone grafts are used to stabilize bone fragments and to immobilize and repair extensive orbital fractures. Open fractures typically are managed by debridement and cleaning of the wound, reduction of displaced by viable bone fragments, and removal of small, grossly contaminated fragments. Depending on the extent of contamination, some or all of the wound is left open for adequate drainage, or drains are placed to facilitate healing. The complete bony orbital rim of the horse generally protects against traumatic globe proptosis, but this problem has been reported on occasion with severe injuries. In most instances, the degree of damage sustained by the orbit and the globe necessitates enucleation. Neoplasia of the equine orbit is less common than that in other domestic species. The most common neoplasia of the posterior orbit are neuroendocrine tumors and extra‐adrenal paraganglioma. Squamous cell carcinoma (SCC) is the most common adnexal tumor that extends secondarily into the orbit (Figure 15.16). Other reported orbital tumors in the horse include anaplastic sarcoma, lymphoma, lipoma, adenocarcinoma, lymphosarcoma, melanoma, meningioma, and others. Progressive exophthalmos, displacement of the nictitans, conjunctival hyperemia and chemosis, orbital swelling, bone surface distortion, blindness, strabismus, anisocoria, behavioral abnormalities, and, less commonly, epistaxis and signs referable to the involvement of adjacent cavities are reported symptoms in horses with orbital tumors. Although surgical removal and salvage of the eye is possible early in the disease process, most cases require exenteration of the orbit. Figure 15.16 Extension of SCC from the eyelids and the nictitans into the orbit. Orbital fat may herniate through weakened episcleral fascia or from trauma, resulting in lobular, subconjunctival masses that may resemble tumors. Aspiration, biopsy, and cytological evaluation of these masses reveal the presence of adipose cells. The affected tissue can usually be excised and the conjunctival and fascia rent closed to prevent recurrence. Entropion is an inward rolling of the eyelid margin. Entropion in adults may be cicatricial from previous eyelid trauma, or it may be acquired or spastic secondary to chronic ocular irritation causing spasms of the orbicularis oculi muscle. Before attempting entropion therapy, concurrent ocular problems such as blepharitis, distichiasis, and corneal disease should be identified and treated. The amount of surgical correction for entropion in mature horses must be estimated before general anesthesia and after local nerve block and a topical anesthetic has been applied to the ocular surface. It is important to determine how much of the entropion is anatomical and how much is secondary to spasm from ocular pain. For optimal results, surgical techniques should always undercorrect slightly. The modified Hotz–Celsus procedure is simple and can be adapted to most types of entropion in the horse. Eyelid trauma and lacerations are common in the horse, especially in young animals. A complete ocular examination is very important to assess corneal integrity, anterior chamber clarity and depth, and scleral continuity since damage to the globe, orbital cellulitis, orbital or periorbital fractures, corneal ulceration, uveitis, hyphema, or posterior segment injuries such as retinal detachment may accompany the lid damage. Damage to the upper eyelid is most significant, however, because most of the globe coverage and protective functions of the eyelids are performed by the upper eyelid. Medial canthal lacerations may result in damage to the nasolacrimal canaliculi. Due to the excellent blood supply to the eyelids, most lacerations can be repaired to achieve a relatively well‐functioning and cosmetic eyelid. Therefore, every attempt should be made to surgically repair all eyelid lacerations, taking care to avoid cutting any hanging eyelid pedicles (Figure 15.17a and b). Failure to repair a laceration, or amputation of a torn eyelid pedicle rather than a surgical repair, can result in exposure‐induced corneal disease. Primary bacterial blepharitis is uncommon in the horse. Eyelid abscesses associated with foreign bodies, SPL lavage systems, and bony sequestra have been reported. Dermatophytosis resulting from Trichophyton or Microsporum sp. may cause blepharitis as well, but usually there are skin lesions elsewhere on the body concurrently. Habronemiasis is a common cause of equine granulomas of the eyelids, conjunctiva, lacrimal caruncle, medial canthus, and nictitans. Infection of periocular tissue by Habronema larvae is a common cause of conjunctivitis or blepharitis. Nonhealing, elevated, and ulcerated periocular granulomas with fistulous tracts and a yellow, caseous exudate (“sulfur‐like” granules) consisting of gritty foci of necrotic mineralized tissue are found on horses during the warm weather months. House and stable flies serve as vectors to transmit eggs and larvae to these warm, moist periocular sites. Cytology from affected sites reveals numerous eosinophils, mast cells, polymorphonuclear cells (PMNs), and plasma cells. Larvae may be identified on histopathology of affected tissue. Topical therapy for solitary, focal lesions of habronemiasis consists of a mixture containing 135 g of nitrofurazone ointment, 30 ml of 90% dimethyl sulfoxide, 30 ml of 0.2% dexamethasone, and 30 ml of 12.3% oral trichlorfon solution. Multifocal lesions should be treated with systemic avermectins and intralesional corticosteroid injections (i.e., triamcinolone) and systemic anti‐inflammatory medications. Figure 15.17 Eyelid lacerations are often full‐thickness and require exact reconstruction. (a) Upper eyelid laceration with a hanging pedicle. This should be reapposed rather than excised. (b) Meticulous apposition of the eyelid margin is critical to postoperative function and comfort, particularly with upper eyelid wounds. Neoplasia of the equine eyelids is very common and can be one of the most challenging periocular diseases to manage. SCC is the most common neoplasm, followed by sarcoids, but a variety of other neoplasms have been reported. Periocular neoplasia, in general, should always be confirmed with histopathology, and treated early and aggressively. Recurrent disease is always more resistant to treatment and is more likely to result in poor cosmesis and compromise of the globe. In advanced cases, especially in untreated chronic SCC, local and distant metastases can occur, resulting in mortality. SCC is the most common neoplasm of the eye and adnexa in the horse. Horses with a lack of periocular pigmentation are at increased risk for development of SCC. An increased prevalence of ocular SCC may occur with age, and a breed predilection for draft breeds and Appaloosas has been reported. Development of SCC is associated with various environmental factors, including geographic influences of increased longitude, decreased latitude, increased altitude, and increased mean annual solar radiation exposure. Ultraviolet radiation is strongly correlated with SCC. Cyclooxygenase (COX)‐derived prostaglandins (COX‐2) may also be responsible for tumor growth, metastasis, and angiogenesis. The most common ocular locations for SCC are the nictitating membrane or medial canthus (approximately 28%) (Figure 15.18), limbus (approximately 28%), and lower eyelid (approximately 23%) (Figure 15.19). Other locations such as the cornea, conjunctiva, and orbit represent approximately 21%. The appearance of adnexal SCC can vary from erosive lesions resembling wounds to proliferative lesions that can be raised and expansive. Actinic solar keratitis may transform to carcinoma in situ SCC that often appears as hyperemic eyelid erosive plaques with dark‐staining crusts, to eventually become papillomatous SCC or, alternatively, SCC may appear as a raised mass with a pink, cobblestone appearance (Figure 15.20
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Equine Ophthalmology
Examination of the Equine Eye
Ocular Problems in the Equine Neonate
Congenital Anomalies and Abnormalities
Microphthalmos
Orbit
Strabismus
Dermoids
Nasolacrimal System Atresia
Corneal Disease
Aniridia
Iridal Hypoplasia and Colobomata
Persistent Pupillary Membranes
Anterior Segment Dysgenesis
Hyaloid Artery Remnants
Cataracts
Congenital Glaucoma
Congenital Disorders of the Posterior Segment
Acquired Ocular and Adnexal Problems in the Foal
Entropion/Ectropion
Eyelid Trauma
Dacryocystitis
Conjunctivitis and Subconjunctival Hemorrhage
Ulcerative Keratitis in Foals
Noninfectious Persistent Corneal Erosions in Neonates
Iridocyclitis in Foals
Equine Orbit
Diagnostic Procedures
Retrobulbar Nerve Blocks
Surgical Techniques for the Orbit
Orbital Inflammation and Cellulitis
Orbital Fractures and Trauma
Orbital Neoplasia
Orbital Fat Prolapse
Diseases and Surgery of the Eyelids
Entropion
Eyelid Lacerations
Blepharitis
Eyelid Neoplasia
Squamous Cell Carcinoma
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