OCULAR TRAUMA Nicholas
Millichamp, BVetMed, PhD, MRCVS
Trauma to the adnexa and globe is a relatively common occurrence in the equine. Ocular injury occurs because of the fractious or excitable nature of horses and the force with which they react to unexpected or unusual situations, whether restrained in stocks, trailers, or simply left to their own devices in a stable or field. Although horses have a closed orbit, the globe is frequently involved in trauma to the orbital area. Many injuries can have devastating consequences for vision if not treated effectively in a timely fashion. Many ocular injuries look worst when seen soon after the traumatic incident occurs. Thorough examination of the eye and adnexa at the time of the injury as well as during the ensuing few days is important. If doubt exists regarding restoring or rreserving vision in a traumatized eye, assume that the eye can be saved and treat it vigorously during the first few days. A severely injured eye can be removed later if subsequent examination indicates that salvage, functionally or cosmetically, is not possible. Factors that suggest an eye is beyond repair include severe lacerations that extend a significant way into the sclera, loss of ocular contents (lens, vitreous), intraocular infection, retinal detachment, and ocular prolapse with severe damage to the extraocular muscles and optic nerve. The prognosis for saving a traumatized eye depends on the type and location of the trauma. The prognosis is better for sharp penetrating injuries to the globe or those that involve only the cornea. The prognosis is worse after perforation or rupture of the globe due to blunt trauma From the Department of Small Animal Medicine and Surgery, Texas A&M University College of Veterinary Medicine, College Station, Texas
VETERINARY CLINICS OF NORTH AMERICA: EQUINE PRACTICE VOLUME 8· NUMBER 3· DECEMBER 1992
or with perforating lacerations extending from the cornea into the sclera. 5
Acute injuries result in the horse being painful and resentful of manipulations around the affected eye. Head shyness can be used to good advantage in assessing the presence or absence of vision. The menace response should be assessed by making careful hand movements toward the affected eye, but avoid exaggerated hand movements to prevent self-trauma. Maze testing is not recommended because a horse with visual impairment is likely to incur further injury by blundering into unseen objects. The direct pupillary light reflex (PLR) may be difficult to assess, particularly in an eye that has a miotic pupil associated with uveitis. A miotic pupil is a reasonable indication that the parasympathetic innervation is intact, however. A dilated pupil in a traumatized eye suggests severe ocular damage and a poor prognosis. The consensual PLR in the noninjured eye, however, is useful in determining the extent of damage to the retina or optic nerve in the injured eye. It often is impossible to visualize these structures because of corneal edema, hyphema, or vitreous hemorrhage. A bright light source directed into the injured eye may be required to elicit a consensual PLR. Either blinking in response to the bright light (prior to applying nerve blocks) or a consensual PLR is an indicator that the retina and optic nerve in the injured eye are still functional. Vitreal hemorrhage, if present, is probably not severe. If no consensual PLR occurs, the prognosis for restoring vision is poor. It is essential that the animal be adequately sedated for ocular examination of the eye. This may not be necessary for animals with chronic, minimally painful injuries. Sedation with xylazine (Rompun, 100 mg/mL, Mobay, Shawnee, KS) administered at 0.4 mg/kg intravenously is suitable in most cases. Butorphanol (Torbugesic, Fort Dodge Laboratories, Fort Dodge, IA), administered at a dose of 0.02 mg/kg intravenously, will provide analgesia if the eye or adnexa is painful. In some cases, detomidine hydrochloride (Dormosedan, 100 f-Lg/mL, SmithKline Beecham, Exton, PA) given intravenously at 20 f-Lg/kg will provide excellent sedation and analgesia. Regional motor nerve blocks facilitate safe examination, especially if any injury has weakened the cornea or sclera. The orbicularis muscle that encircles the palpebral fissure is innervated by the auriculopalpebral branch of the facial nerve. This muscle is capable of strong eyelid closure that can exert considerable pressure against the cornea or sclera weakened by laceration or ulceration. A block of the auriculopalpebral nerve can be performed along the zygomatic arch, halfway between the lateral canthus of the eye and the base of the ear. The nerve can usually be palpated crossing the superior margin of the arch at this
point. The auriculopalpebral nerve can also be blocked farther caudally, in the depression formed by the intersection of a vertical line drawn dorsally along the posterior border of the ramus of the mandible and a line drawn caudally along the superior edge of the zygomatic arch. The nerve cannot be palpated at this site. Regional anesthesia of ocular sensory innervation is not usually important for examination, but can be used to allow insertion of a subpalpebral lavage system. Blocking the frontal branch of the trigeminal nerve, emerging from the supraorbital foramen dorsal to the upper orbital rim, provides anesthesia to the skin of the upper eyelid. The foramen is palpated as a depression 2 to 4 em superior to the orbital rim. Topical application of local anesthetic such as proparacaine hydrochloride (Ophthaine, E.R. Squibb, Princeton, NJ) to the cornea and palpebral conjunctiva reduces pain due to corneal abrasions and is required for subpalpebrallavage system placement. Further information on examination techniques and nerve blocks may be found in the article by Cooley, and guidelines for treatment in the article by Miller. The injured eye and adnexa frequently are difficult to examine soon after trauma due to massive tissue swelling (blepharoedema and chemosis). Chemosis and subconjunctival hemorrhage may be so severe as to prevent the globe being seen at all (Fig. 1). In such cases, it may be difficult to assess the extent of injury to the globe itself. With the horse sedated and following regional nerve blocks, the lids should be opened and the conjunctiva deflected to view the globe. If this cannot be performed without risk of injury to the eye, it is best to begin therapy with antibacterial and anti-inflammatory drugs and reassess the situation several hours later or be prepared to administer general anesthesia for better evaluation and to institute immediate surgical repairs as needed. In less severe ocular injury cases, a twitch may facilitate examination of painful and fractious horses.
Figure 1. Ventrolateral deviation of the globe, with chemosis and subconjunctival hemorrhage.
The ocular examination should proceed from the anterior to posterior segment, examining lids, orbital structures, conjunctiva, cornea and sclera, anterior chamber, lens, and retina.
ADNEXAL TRAUMA Eyelid Injuries
The eyelids should be evaluated for contusions, lacerations, or puncture wounds. The periocular tissues are palpated for swelling, emphysema (indicating fractures involving the paranasal sinuses), and crepitus due to orbital fractures. It is useful to view the eyes and eyelids from in front of the horse and to palpate the eyes and periocular tissues at the same time to judge any loss of symmetry. The conjunctival fornices and bulbar surface of the third eyelid should be examined for lacerations and foreign bodies. Swollen eyelids associated with traumatic injuries may preclude eyelid closure. This should be assessed to determine what corneal protection is required. Blunt trauma to the eyelids usually causes blepharoedema, chemosis, and subconjunctival hemorrhage. In the absence of other orbital or globe involvement, therapy with systemic nonsteroidal anti-inflammatory drugs (NSAIDs) such as flunixin meglumine (Banamine, Schering, Kenilworth, NJ) administered intravenously or orally, 1.1 mg/kg daily, is effective in reducing swelling and providing analgesia. Dimethyl sulfoxide (Domoso Solution, Syntex Animal Health, San Diego, CA) may be applied to the eyelids to reduce blepharoedema and ocular exposure. Cold compresses may be used in the immediate post-traumatic period if the horse will tolerate them. Lacerations of the eyelids are common injuries in the horse. It is important to assess whether the globe is involved in such injuries. Lacerations that do not involve the margin of the eyelids are easily repaired under sedation and local anesthesia using simple interrupted sutures of nylon or silk. If the eyelid margin is also lacerated, it is imperative to repair the margin as soon as possible to restore its normal anatomy. For small lacerations, only the outer skin-orbicularis layer of the lid requires suturing. If the laceration is extensive, a two-layered repair is needed. The deeper tarsoconjunctiva should be sutured with absorbable suture-5-0 to 6-0 polyglactin 910 (Vicryl, Ethicon, Somerville, NJ)-as one layer using a simple interrupted or continuous pattern, taking care to avoid suture penetrating the conjunctival surface and ensuring that the knots are buried within the lid. The outer skin orbicularis layer is sutured with nonabsorbable material (4-0 or 6-0 silk). Suture the eyelid margin first to achieve exact apposition of the margin tissues. For the outer skin-orbicularis layer, a marginal cruciate (figure of eight) suture ensures exact marginal apposition. Simple interrupted sutures are used to complete the repair. Failure to repair an eyelid laceration-particularly on the upper lid-correctly results in
cosmetic disfigurement, impaired tear film distribution, and corneal irritation (Fig. 2). Even quite large eyelid lacerations can be sutured in the standing sedated horse. If the animal is fractious, general anesthesia should be used. The latter is essential if extensive lacerations result in loss of tissue or if there is a delay in treating the laceration, resulting in tissue contraction that requires sliding skin flaps or other blepharoplastic procedures. Eyelid sutures should be left in place for at least 10 days. In the absence of other ocular injuries, topical antibiotic ointments should be applied to the cornea after surgery to reduce corneal irritation during healing of the eyelids. Systemic NSAIDs should be administered. Systemic antibiotics may be used for several days, especially if there is any delay in repairing the laceration or if there is any appearance of infection at the site of the injury. All horses with eyelid lacerations should receive tetanus prophylaxis. Eyelid lacerations presented a few days after injury need judicious debridement of the laceration margins; care should be taken to debride as little tissue as possible. The eyelids have an excellent blood supply. Removal of large amounts of lid tissue is not necessary, makes it difficult to restore a normal cosmetic appearance, and may result in corneal exposure, cicatricial entropion, or ectropion. Large flaps of eyelid tissue can usually be sutured back into normal apposition, even when the repair is delayed. Lacerations involving the nictitating membrane should be sutured if they involve the margin. The conjunctiva can be sutured with 6-0 polyglycolic acid (Dexon, Davis and Geck, Manati, PR), polyglactin 910, or polydioxanone (PDS, Ethicon). If the nictitans is severely damaged,
Figure 2. Failure to suture the eyelid margin correctly has resulted in inadequate cosmesis after this eyelid laceration.
it may be removed. Foreign bodies occasionally become trapped behind or penetrate the nictitans. These can be removed and defects sutured if extensive. Periocular puncture wounds carry the potential for development of retrobulbar and periocular cellulitis or abscess formation. These should be treated vigorously with systemic antibacterial and antiinflammatory drugs and tetanus prophylaxis.
The equine globe is protected by an enclosed bony orbit. The orbital bones may be damaged by kicks, collisions with hard objects, or heavy blows to the face. Fractures of the ventral wall of the orbit and frontal process of the zygomatic bone are relatively common and may entrap ocular structures. Fractures of the orbit or orbital soft tissue injury may result in severe retrobulbar and subconjunctival hemorrhage. Corneal and scleral lacerations, uveitis, and ocular contusion may accompany orbital fractures. Damage to the orbital bones may be discerned by facial asymmetry, crepitus, subcutaneous emphysema, or compound fractures. If there is any suspicion of trauma involving the orbital bones, radiography is indicated to assess the extent of damage. Orbital radiography, however, is difficult to interpret in horses because of the extensive nasal and sinus structures. Lateral, dorsoventral, and oblique views of the orbit can be obtained with sedation or ventrodorsal views with general anesthesia. The oblique view is usually most revealing. 7 If the globe is not involved, orbital fractures need not be reduced surgically immediately, but may be managed conservatively until initial swelling has subsided. If the globe is involved, it may be necessary to remove bone fragments or reposition bone fragments that are exerting pressure on the globe or optic nerve or trapping the extraocular muscles and limiting ocular motility. The goals of initial therapy are to reduce inflammation, swelling, and pain with systemic NSAIDs such as flunixin meglumine. Systemic antibacterial drugs are indicated, especially if compound fractures are present. With severe eyelid swelling, the eyelids may not close, predisposing the cornea to drying and exposure keratitis. This may be compounded if periocular trauma or fractures interfere with or transect the palpebral branch of the facial nerve. Artificial tears (Tears Naturale II, Alcon Laboratories, Fort Worth, TX) and lubricating petrolatum ointment (Lacri-Lube, Allergan Pharmaceuticals, Irvine, CA) applied to the conjunctiva and cornea keep the exposed surface moist until swelling around the eye subsides. Corticosteroids may be given systemically provided no evidence of corneal ulceration is detected. Minor orbital fractures usually are not treated surgically provided facial asymmetry is minimal. Severe comminuted fractures with displacement of bony fragments can be repositioned using interosseous
wiring techniques and bone grafts. 2, 4 Zygomatic bone fractures can be repaired using open techniques or, in the case of closed fractures, a closed technique using a bone hook inserted into the conjunctival fornix to pull bone fragments back into apposition. 1 Ocular movements are rarely affected in the horse unless there is muscle entrapment. The enclosed bony orbit reduces the chance of ocular proptosis. In any case in which ocular motility is limited or any evidence of proptosis is seen, however, it should be assumed that there is either muscle damage or damage to the extraocular innervation (Le., the oculomotor and abducens nerves). The prognosis in such cases is guarded. Facial Nerve Injuries
Trauma to the head or skull fractures may involve the facial nerve, causing an inability to blink and reduced tear production. Corneal exposure may result in keratitis and ulceration. The prognosis for recovery of eyelid and lacrimal gland function after these injuries is poor. Therapy consists of topical artificial tears (Tears Naturale II) and ointment (Lacri-Lube) to maintain corneal wetting and lubrication. Temporary split-thickness tarsorrhaphy sutures can be used to protect the cornea and facilitate healing. A permanent partial medial or lateral tarsorrhaphy occasionally may be required to reduce the length of the palpebral fissure, thus preventing corneal exposure. GLOBE AND OPTIC NERVE TRAUMA Corneal and Scleral Lacerations
The cornea should be examined for any change in clarity or surface contour. Any evidence of corneal irregularity should be evaluated by fluorescein staining to determine the presence and extent of corneal abrasions or lacerations. Blunt trauma to the cornea that fails to cause abrasion or laceration may cause damage to the posterior endothelium of the cornea and result in corneal edema. Iridocyclitis usually accompanies the corneal injury. Treatment for uveitis is outlined subsequently, with more detailed treatment options given in the article by Schwink. The severity of the corneal injury initially depends on the nature of the traumatic event. Subsequently, progression and worsening of the problem may reflect inadequate therapy or ocular infection. Superficial corneal lacerations may consist of an area of surface irregularity or a flap of corneal tissue. With deep nonperforating injuries, the edges of the laceration gape and the adjacent cornea is thickened by corneal edema. If a corneal laceration perforates, it usually is obscured by a protruding gray or hemorrhagic gel-like mass of secondary fibrinous aqueous, often containing brown iris tissue. It is
important to assess the anterior chamber for depth and extent of hemorrhage. If possible, determine whether the lens has been lacerated or lost. Inspect the full length of the laceration, especially those extending across the cornea into sclera. This is often difficult in the conscious horse. Superficial corneal abrasions involve epithelial loss and, occasionally, some corneal stromal damage or loss. The eye is painful and characterized by conjunctival injection, chemosis, corneal irregularity, and corneal opacification due to edema (Fig. 3). Ocular pain arises from the corneal injury and associated anterior uveitis. Uveitis occurs because of an axon reflex between the densely innervated cornea and the anterior uvea. If corneal injury is difficult to examine, fluorescein dye will stain the area of the abrasion. Acute corneal abrasions can be treated empirically with topical antibacterial agents such as neomycin sulfate, polymyxin B sulfate, and gramicidin (Neosporin, Burroughs Wellcome, Raleigh, NC) applied three to four times daily. Atropine, 1% to 3%, should be applied two to four times daily to achieve mydriasis and cycloplegia. Systemic NSAIDs such as flunixin meglumine (Banamine) or ketoprofen (Keofen, Fort Dodge Laboratories) reduce pain and help control uveitis. Corticosteroids should never be used in cases of corneal abrasions because of their tendency to reduce the rate of epithelial healing and potentiate infection with bacteria or fungi. There usually is no need to perform conjunctival flaps or place third eyelig flaps for superficial abrasions provided they are medicated vigorously. Even minor traumatic corneal abrasions should be checked frequently during treatment to ensure that uncomplicated healing occurs, however. Corneal abrasions disrupt the outer protective epithelial layer and may predispose the eye to infection with various gram-negative bacteria such as Pseudomonas spp. or fungi such as Fusarium spp. and Aspergillus spp. Influx and degranulation of polymorphonuclear leukocytes in response to infection can result in rapid breakdown of the corneal stroma, which, if unchecked, will result in progression to deep corneal
Figure 3. A superficial abrasion of the cornea.
ulceration and even corneal perforation. In cases of abrasions resulting in corneal ulceration and stromal dissolution (melting), the lesion should be cultured and treated vigorously with fortified antibiotics. There is a shift from gram-positive to gram-negative organisms in many cases of conjunctivitis or keratitis. Antibiotics such as gentamicin, tobramycin, and amikacin may be more appropriate in cases of corneal abrasions that do not respond to initial antibiotic treatment. Topical therapy through a subpalpebrallavage system using fortified antibiotics (formulated in artificial tears by adding injectable gentamicin, tobramycin, or amikacin to achieve a concentration of 0.6%-1 % or 6-10 mg of active antibiotic per milliliter of artificial tears) administered every 2 hours is recommended. Combinations of aminoglycoside and penicillin antibiotics administered using an alternating regime may be useful in cases of rapidly progressing corneal ulceration secondary to ocular trauma. Fortified solutions of amikacin and ticarcillin may be alternated and instilled every 2 to 4 hours, for example. 8 Other medications that may help reduce stromal melting include autologous serum containing anticollagenolytic macroglobulin and acetylcysteine. In the author's experience, acetylcysteine does not significantly alter progression of the ulcer and may result in marked disruption of the tear film by disrupting the deep mucous layer. Conjunctival flaps occasionally are useful in cases of deep corneal ulceration. Third eyelid flaps should not be used in cases of deep corneal ulceration. Further specific information on corneal ulcer management can be found in the article by Nasisse and Helms. In some corneal injuries, a flap of corneal stroma and epithelium may be displaced. Provided the flap is still attached at some point on the cornea, it should be sutured back to the underlying stroma with half-thickness simple interrupted sutures of 7-0 polyglycolic acid or polyglactin 910. Sutures must be anchored to healthy or vascularized stroma; if the cornea is weakened by stromal melting, sutures will not adequately maintain tissue apposition. Corneal lacerations should be sutured using general anesthesia. Lacerations of the corneal stroma that penetrate the stroma but do not perforate the cornea are sutured with simple interrupted sutures of 7-0 polyglycolic acid or polyglactin 910. The depth of the sutures is determined by the depth of the laceration, but should not incorporate the inner endothelial corneal surface. Sutures should be placed 1 to 2 mm apart. If the laceration is sutured correctly, conjunctival or third eyelid flaps are not necessary following corneal repair. Protective flaps and temporary tarsorrhaphies should be avoided because they prevent adequate topical medication of concurrent keratitis or uveitis. Covering the globe with a third eyelid flap or tarsorrhaphy also prevents evaluation of corneal healing. Penetrating corneal lacerations that extend across the limbus into the bulbar conjunctiva and sclera should be evaluated carefully to ensure that no scleral perforation is involved. Perforating lacerations of the cornea typically have associated iris prolapse, anterior chamber collapse, and severe iridocyclitis. At the moment of perforation, the iris is carried into the wound by escaping
aqueous humor. Tissue damage causes breakdown of the bloodaqueous barrier and massive influx of protein, including fibrinogen, into the anterior chamber. Fibrin formation produces a temporary seal around the plug of iris. Trapped iridal tissue has a dark brown color. Fibrinous (secondary) aqueous and clotted blood frequently are seen protruding above the corneal surface around the laceration. The amount of fibrinous aqueous on the corneal surface is a poor guide to the lesion's severity; the laceration often is smaller than the bleb of secondary aqueous on the corneal surface. Iridocyclitis is present in all perforating lacerations. The pupil is miotic and the anterior chamber, if reformed, may be shallow and may contain fibrin, hyphema, and inflammatory cells. In cases of severe perforating lacerations, the cornea needs to be explored thoroughly and repaired using general anesthesia. Preoperative medications to treat the keratitis and uveitis include topical and systemic broad-spectrum antibiotics, 1 % topical atropine, and systemic NSAIDs. During surgery, carefully explore beneath the plug of secondary aqueous and iris to determine the laceration's length and shape. Identify any progression of a perforating laceration into the sclera. Failure to repair the latter results in chronic aqueous leakage and phthisis (shrinkage) of the globe. To repair a perforating corneal laceration, the iris should be separated from the margins of the laceration and repositioned in the anterior chamber, and the cornea (and sclera) repaired with 7-0 polyglycolic acid or polyglactin 910. If the lesion is less than 24 hours old, the iris most likely can be replaced intact. If the lesion is older than this, any devitalized tissue should be trimmed carefully with scissors until hemorrhage is detected and then the iris replaced in the eye. Irregularly shaped lacerations should be sutured to create several short linear wounds. The resulting short segments are then closed carefully, avoiding tissue distortion or buckling. Reform the anterior chamber with lactated Ringer's solution, viscoelastic materials such as sodium hyaluronate (Healon, Pharmacia Ophthalmics, Pasadena, CA, Alcon Surgical, Fort Worth, TX), hydroxypropyl methylcellulose (Keragel, The Cutting Edge Ltd, Diamond Springs, CA), sodium chondroitin sulfate-sodium hyaluronate (Viscoat) or an air bubble. These are injected into the anterior chamber through the partially closed incision to displace the lens and iris posteriorly, thus reforming the anterior chamber. Viscoelastic materials protect the corneal endothelium and can be used throughout the surgery. The cost for quantities needed in horses may be prohibitive, however. Large volumes of air left in the eye after surgery may damage the corneal endothelium and air or viscoelastics should be replaced with lactated Ringer's or balanced salt solution (8.5.5., Alcon Laboratories) immediately before placing the final suture in the cornea. Postoperative therapy should continue as before surgery. At the time of corneal repair, a subpalpebral lavage tube placed through the upper eyelid facilitates topical application of solutions. 3 Administer topical antibiotics at least every 6 hours, systemic antibiotics twice daily, and topical atropine every 6 to 24 hours. In many cases, 1 % atropine
is adequate, although 3% may be used in adult horses. If atropine is used, administer only enough to achieve a dilated pupil. Systemic NSAIDs should be continued postsurgically for at least the first few days. Because complicated corneal lacerations heal by corneal vascularization and scar formation, use of NSAIDs should be discontinued once the eye is comfortable because they slow vascularization of the cornea. If postoperative uveitis is severe, systemic corticosteroids carefully may be used instead of NSAIDs. Foreign Bodies
Ocular trauma may result in foreign bodies becoming lodged in the eye. Penetrating and perforating corneal foreign bodies should be removed and the defect sutured. Medical therapy should include topical and systemic antibiotics, a mydriatic/cycloplegic drug, and NSAIDs systemically. In view of the potential risk of bacterial or fungal organisms being inoculated into the cornea or globe with the foreign body, corticosteroids should not be used in such cases. In cases of gunshot wounds to the eye, pieces of shot may be lodged inside the eye or its coats. Metallic foreign bodies can be localized by radiography. A metal Flieringa's ring sutured to the periphery of the limbus serves as a landmark for exact foreign body location determination. Both metallic and nonmetallic foreign bodies may be located with B-mode ultrasonography using 7.5- or lO-MHz transducer probes. A foreign body within the anterior segment can usually be removed surgically without complication. Foreign bodies located in the vitreous can be removed through the ciliary body pars plana, although this is a difficult technique requiring specialized training and instrumentation. For optimal case management, ocular injuries associated with anterior or posterior segment foreign bodies should be referred to a veterinary ophthalmologist. Uveitis
Inflammation of the anterior uvea, comprising iris and ciliary body (iridocyclitis), or inflammation involving the posterior segment (chorioretinitis) often accompanies ocular trauma. Anterior uveitis may be seen with concussive injuries to the globe or penetrating or perforating injuries to the cornea. Characteristic signs include conjunctival injection, corneal edema, aqueous flare (protein and cells in the aqueous humor), anterior chamber fibrin or hemorrhage, and a miotic pupil, often with iris swelling. Posterior synechiae (adhesion of the posterior iris surface to the anterior lens capsule) may develop. Cells or hemorrhage in the anterior vitreous commonly obscure the retina. If the retina is difficult to visualize by ophthalmoscopy, involvement of the posterior segment should be suspected. Sequelae of uveitis include synechiae, cataract, retinal degeneration, and retinal detachment.
SUbpalpebral lavage is often the easiest way to treat a horse with uveitis, provided the upper eyelid has not been traumatized. Topical corticosteroids can be used provided there is no evidence of corneal epithelial damage (i.e., no fluorescein dye staining). Dexamethasone, 0.1 % (Maxidex, Alcon Laboratories), or prednisolone acetate, 1% (EconoPred Plus, Alcon Laboratories), suspensions should be instilled every 4 to 6 hours. These may be combined with topical antibiotics such as neomycin and polymyxin B (Maxitrol Ophthalmic Suspension, Alcon Laboratories). If no corneal damage exists, topical antibiotics may not be necessary. Atropine should be used for mydriasis, to reduce the potential for synechiae formation, and for cycloplegia, to reduce painful ciliary muscle spasm. Horses are less likely to suffer self-inflicted ocular trauma if atropine is used. Atropine (1 %-3%) should be used every 6 hours until mydriasis occurs, then the frequency of administration decreased. If mydriasis can be maintained with 1% atropine infrequent administration, there is no need for more frequent treatment. Topical atropine may cause intestinal stasis in horses, although colic associated with topical atropine use appears to be uncommon. Inflammation control and analgesia can be achieved with systemic NSAIDs. Acute treatment with flunixin meglumine (Banamine) administered intravenously or orally (1.1 mg/kg) is particularly effective in limiting ocular inflammation. Aspirin, 25 mg/kg twice daily for 3 to 5 days and then 30 mg/kg once daily, or phenylbutazone, 2 to 4 mg/kg once daily, may be used for long-term treatment. 6 Flurbiprofen, 0.03% (Ocufen, Allergan Pharmaceuticals), is not licensed for use in the horse, but the author finds it useful in limiting ocular inflammation postsurgically or in other cases of uveitis. One to two drops applied to the cornea or administered via subpalpebral lavage four times daily is effective. Long-term use of topical flurbiprofen, however, is an expensive proposition in the horse. Systemic prednisone may be given orally, 0.5 to 2 mg/kg for 7 to 21 days. Specific aspects of uveitis treatment are covered in the article by Schwink. Lens Injuries
The lens may be directly involved in ocular trauma. Injuries that perforate the globe may cause lens capsule rupture and lens protein release. The resultant uveitis is often severe and refractory to treatment. Vision and globe integrity frequently are lost. If a lens capsule rupture is present, the horse immediately should be referred to a veterinary ophthalmologist for lens removal. Lens removal by phacofragmentation and aspiration is the only effective way to save an eye with lens rupture. If the anterior lens capsule cannot be evaluated because of hemorrhage or fibrin in the anterior chamber, lens rupture should be suspected in any case of perforating ocular injury with a rapid deterioration in the eye over a 2- to 3-day period, despite vigorous antiinflammatory therapy. The prognosis for restoration of vision or for saving a cosmetic eye is guarded in these cases.
Figure 4. A traumatic luxation of a microphakic lens.
Lens luxation in the horse occurs most commonly as a sequel to equine recurrent uveitis or glaucoma. In cases of blunt trauma, the lens may be dislocated. Posterior luxations are seen most frequently. Considerable force is needed to luxate the lens in a normal eye and traumatic lens luxation is therefore accompanied by signs of severe injury (i.e., hemorrhage, severe uveitis, and retinal detachment). Lens luxation occasionally occurs with mild trauma, although there may be predisposing causes such as microphakia (Fig. 4). Whereas an anterior lens luxation may be directly visible on examination, posterior lens luxation into the vitreous may be difficult to see if ocular hemorrhage is present. Lens luxation in the horse should be treated conservatively. Associated uveitis requires vigorous anti-inflammatory therapy. An anteriorly luxated lens may be removed surgically by a veterinary ophthalmologist, although the prognosis in such cases is guarded. In some cases of perforating corneal injury, lens and vitreous loss occurs at the time of injury. In this instance, the prognosis for saving a visual eye is very poor because other ocular damage, including retinal detachment, is likely. If the corneal laceration appears to be repairable, a better course of treatment is to perform a surgical evisceration by removing the ocular contents and inserting a silicone sphere before repairing the cornea and sclera. Otherwise, globes with trauma severe enough to cause loss of the lens and possibly vitreous are candidates for enucleation.
Hemorrhage in the vitreous arises from the ciliary body, retinal blood vessels, or choroid. Hemorrhage in the vitreous appears as a reddish haze behind the lens. Vitreal hemorrhage resorbs more slowly
Figure 5. Optic atrophy and retinal degeneration following severe head trauma.
than anterior chamber hemorrhage and may compromise vision in an otherwise normal eye. Hemorrhage and fibrin in the posterior vitreous often organize into fibrous strands that exert traction on the retina. Detachment, partial and complete, is common. Extensive hemorrhage in the vitreous can be treated by surgical vitrectomy, although this is not a commonly-performed procedure in the horse.
The posterior segment of the eye should be examined, whenever possible, using indirect ophthalmoscopy to rule out retinal inflammation, retinal detachment, vitreous or retinal hemorrhage, and optic nerve inflammation or atrophy. In many cases, corneal edema, hyphema, and anterior chamber fibrin obscure a view of the posterior segment. If the eye has not suffered a perforating injury, ultrasonography should be used for noninvasive evaluation of the posterior segment. Retinal edema may occur in traumatized eyes. Clinically, it appears as grey-white streaks throughout the nontapetal fundus. Areas of apparently raised retina with fuzzy edges may be seen in the tapetal fundus. Retinal edema occasionally is associated with optic nerve injuries. Retinal edema is treated with systemic NSAIDs and corticosteroids. Depending on the duration and severity of the edema, resolution may be associated with focal areas of retinal degeneration. Retinal detachment in the horse may result from ocular trauma,
although it is more commonly a sequela of equine recurrent uveitis. The extent of the detachment depends on the severity of the trauma. If the retina becomes torn, vitreous may migrate beneath the retina, causing progressive detachment. Clinical signs depend on the severity of the detachment. A partial detachment may cause little noticeable vision loss, whereas a total detachment causes blindness. The pupil may be dilated and nonresponsive or partially responsive to light. Partial peripheral detachment will be seen only with ophthalmoscopy, whereas total detachments resemble a white or gray sheet behind the lens. Retinal detachments should be treated medically with systemic corticosteroids and NSAIDs. Surgical therapy has not been attempted in the horse, and the prognosis for most retinal detachments is poor.
Traumatic Optic Neuropathy-Optic Atrophy
The equine optic nerve appears to be quite a sensitive site for the effects of traumatic head injuries. It has been suggested that certain types of head injury, especially blunt trauma to the back of the head, result in posterior movement of the brain, causing neuropraxia of the intracranial optic nerve that is fixed in position by the optic canal. This is a common problem in the horse that rears and falls over backwards, or rears up and strikes the occipital region. Horses thus affected present with a sudden onset of unilateral or bilateral blindness that may be detected immediately after or within a few days of the injury. An afferent PLR deficit will be present. The fundus may initially appear normal or hemorrhage may be seen over an edematous optic nerve. After several weeks, the optic nerve becomes pallid and the reticular outline of the scleral lamina cribrosa is evident (Fig. 5). The peripapillary blood vessels are attenuated and eventually lost and peripapillary retinal depigmentation (atrophy) is seen. Horses that present with acute traumatic blindness and a normal ophthalmoscopic examination should be treated with systemic corticosteroids and NSAIDs, although the prognosis for restoration of vision is poor. Vigorous anti-inflammatory therapy occasionally maintains vision. 6
References 1. Blackford JT, Hanselka OV, Heitmann JM, et al: Noninvasive technique for reduction of zygomatic process fractures in the horse. Vet Surg 14:21-26, 1985 2. Caron JP, Barber SM, Bailey JV, et al: Periorbital skull fractures in five horses. J Am Vet Med Assoc 188:280-284, 1986 3. Oziezyc J, Millichamp NJ: Infectious ocular diseases. In Smith B (ed): Large Animal Internal Medicine. St Louis, CV Mosby, 1990, P 1215-1237 4. Koch DB, Leitch M, Beech J: Orbital surgery in two horses. Vet Surg 9:61-65, 1991 5. Lavach JO, Severin GA, Roberts SM: Laceration of the equine eye. A review of 48 cases. J Am Vet Med Assoc 184:1243-1248, 1984
6. Rebhun WC: Traumatic optic neuropathy. How to prevent permanent blindness. Vet Med 81:350-353, 1986 7. Turner LM, Whitley RO, Hager 0: Management of ocular trauma in horses. II. Orbit, eyelids, uvea, lens, retina and optic nerve. Mod Vet Pract 67:341-347, 1986 8. Whitley RO, Turner LM: Management of ocular trauma in horses. I: Cornea and sclera. Mod Vet Pract 67:233-238, 1986
Address reprint requests to Nicholas J. Millichamp, BVetMed, PhD, MRCVS Department of Small Animal Medicine and Surgery Texas A&M University College of Veterinary Medicine College Station, TX 77843