Ophthalmic Anatomy

Like many prey species, rabbits have large, laterally placed eyes. The angle between their orbits is 150 to 175 degrees, allowing a visual field of almost 360 degrees. Their stereoptic vision is poor, with only 10 to 35 degrees of binocular overlap. The orbit contains a large venous sinus, extending from the orbital apex to the globe equator and draining posteriorly to the pterygoid and cavernous sinuses. This extensive vascular network within the orbit is a common cause of significant hemorrhage during enucleation.

The nasolacrimal apparatus of the rabbit is unique. Although rabbits only blink once every 5 to 6 minutes, their tear film remains stable and they rarely have exposure keratitis secondary to evaporation. Tear film stability is likely enhanced by the presence of four orbital glands: the lacrimal gland, an accessory lacrimal gland with retrobulbar, orbital, and infraorbital lobes, superficial gland of the third eyelid, and deep gland of the third eyelid (harderian gland). Retention of the lacrimal lake may be facilitated by the lack of a superior lacrimal puncta, which would result in a slower rate of tear clearance. The nasolacrimal duct follows a tortuous route through the lacrimal and maxillary bones and passes in close proximity to the apices of the molar and incisor teeth before emerging through the nasal mucosa. Owing to several sharp bends and associated duct narrowing, blockage of the duct and subsequent dacryocystitis is common.

The most remarkable anatomic difference of the rabbit eye from that of other species is its retinal vascular pattern. Lagomorphs are the only species with a merangiotic fundus, in which the retinal blood vessels radiate horizontally from the optic disc, running with the myelinated nerve fiber layer. The optic disc is situated in the superior fundus and thus requires that the examiner use an upward gaze to view the optic disc. An obvious central depression in the optic disc (physiologic cup) is apparent secondary to lack of a developed lamina cribrosa and extensive myelination of optic nerve axons at that point. This appearance can be challenging to distinguish from glaucomatous cupping of the optic nerve head.

Orbital Disease

Exophthalmos is the most prevalent clinical sign associated with orbital disease. In rabbits, retrobulbar abscesses are commonly the cause of exophthalmos (Figure 20-1). Pasteurella multocida has frequently been implicated as the cause for these abscesses, although confirmation through culture is rarely attained. Regardless of the specific pathogen responsible, it likely gains access to the orbit either through infected molar tooth roots or from hematogenous spread. Diagnosis is made through clinical signs and ocular ultrasonography. Successful treatment is difficult. The abscess cannot be drained through the oral cavity because of the rich vascular plexus lining the rabbit orbit as well as the extremely caseous nature of the contents. Many cases require exenteration and long-term medical therapy with a broad-spectrum antibiotic. True Pasteurella-induced abscesses may respond favorably to parenteral penicillin therapy at a dose of 60,000IU/kg q24h for several weeks. However, the use of penicillins in rabbits warrants extreme caution because they can cause anaphylaxis or fatal enterocolitis due to alteration of the normal gastrointestinal flora. Even with aggressive surgical and medical therapy, many of these abscesses recur and at times necessitate euthanasia. Less common causes of exophthalmos in rabbits include parasitic cysts, orbital neoplasia, and metastatic thymoma.

Figure 20-1 Marked exophthalmos of the right eye of a rabbit secondary to a large retrobulbar abscess. Culture of the abscess was negative for aerobic and anaerobic organisms.

Adnexal Disease

Adnexal disease is uncommon in rabbits, with entropion being the most commonly observed abnormality. Entropion may involve the upper and/or lower eyelids and may be primary or secondary. Primary (congenital) entropion has been described in the New Zealand white and French lop breeds. These breed predispositions suggest an inherited basis, but a mode of inheritance has not been determined. The lower eyelids are most commonly affected in New Zealand white rabbits, whereas the upper eyelids are affected in French lops. Clinical signs associated with primary entropion include epiphora, blepharospasm, conjunctival hyperemia, and, sometimes, ulcerative keratitis (Figure 20-2). Application of a topical anesthetic such as 1% proparacaine will facilitate ophthalmic examination by alleviating surface ocular pain. It will also remove any spastic component to the entropion, allowing appropriate surgical planning. Correction of entropion with a modified Hotz-Celsus procedure allows restoration of normal anatomic conformation, thereby preventing further ocular irritation.

Figure 20-2 Entropion of the right upper eyelid of a rabbit with secondary ulcerative keratitis.

Entropion may occur from cicatrix formation secondary to chronic blepharitis or blepharoconjunctivitis. Before any attempt at surgical correction, the underlying cause must be identified and treated. Otherwise entropion will likely recur. Cicatricial entropion is corrected using a Y-to-V blepharoplasty, with care taken to completely excise the offending fibrotic tissue during the procedure. Infectious blepharitis may result from exposure to Treponema cuniculi, or rabbit syphilis (Figure 20-3). T. cuniculi is a spirochete bacillus transmitted by infected dams. The most commonly affected areas are the vulva, prepuce, lips, nares, and anus. Clinical signs include thickening, crusting, and, possibly, ulceration of the eyelid. Diagnosis is confirmed through identification of spirochetes in biopsy or skin scraping samples. Darkfield microscopy enhances visualization of the organism. Three doses of parenteral benzathine penicillin G or procaine penicillin G at a dose of 42,000IU/kg at 7-day intervals is the treatment of choice. Careful monitoring of the patient for potentially fatal enterocolitis is necessary. Blepharitis may also be caused by self-induced trauma or maceration due to ocular discharge secondary to dacryocystitis, conjunctivitis, or keratitis (discussed later).

Figure 20-3 Marked blepharitis and severe mucopurulent ocular discharge in a rabbit with Treponema cuniculi.

Neoplasia of the eyelids is rarely reported in the rabbit. The most common tumors of the eyelid are squamous cell carcinoma, fibrosarcoma, and melanoma. Squamous cell carcinoma must be differentiated from treponemal blepharoconjunctivitis, because both can have similar clinical presentations. Diagnosis is made through biopsy, preferably excisional biopsy, which may be curative in cases of squamous cell carcinoma. If diffuse disease prevents complete excision, adjunctive therapy with β-irradiation or cryotherapy may be used. If these modalities are not available, referral or enucleation is recommended. Fibrosarcoma manifesting in the eyelid may represent extension from the orbit. Careful examination, including globe retropulsion as well as advanced imaging using computed tomography (CT) or magnetic resonance imaging, may aid in distinguishing the extent of tumor involvement. Orbital involvement carries a guarded prognosis. Exenteration may be palliative and may increase survival time. Melanomas of the eyelid tend to be benign although locally invasive. Surgical excision is curative.

Conjunctival Disease

Conjunctivitis may be a primary clinical sign but is frequently associated with blepharitis or keratitis. Noninfectious causes of conjunctivitis include keratoconjunctivitis sicca, trauma (self-induced or due to foreign bodies such as straw, dust, seed husks), and environmental allergens. Keratoconjunctivitis sicca is uncommon, is diagnosed with the aid of a Schirmer tear test with accompanying clinical signs, and is frequently the result of chronic conjunctivitis. Treatment consists of artificial tear replacement therapy.

Bacteria and viruses are commonly present in infectious conjunctivitis; however, fungi are rarely encountered. Offending bacteria may represent overgrowth of the normal conjunctival flora and include Staphylococcus aureus, P. multocida, Haemophilus spp., Pseudomonas spp., and Chlamydia spp. Treatment should be based on results of culture and sensitivity testing but frequently includes topical chloramphenicol or ciprofloxacin used long term. Relapses are common, and the addition of systemic antimicrobial agents may be necessary.

Viral causes of ophthalmic disease are relatively uncommon in domestic rabbits in the United States. Myxoma virus is a member of the Poxviridae family and is endemic in the western United States (especially among brush rabbits in California), Europe, and Australia. The virus is transmitted by an arthropod vector, including both mosquitoes and fleas. Clinical signs are blepharoconjunctivitis with a thick mucopurulent discharge, blepharedema, and edema and nodule formation on the ears, head, body, and limbs. Myxoma virus was formally thought to have 100% mortality, but more recent data suggest that the prognosis varies according to the strain of the virus and species/breed of rabbit. Diagnosis is obtained from clinical signs, gross pathology findings, and polymerase chain reaction (PCR) analysis of tissue extracts. Treatment is supportive only.

Rabbit fibroma virus has also been responsible for the formation of flat, subcutaneous tumors of the periocular skin. Similar to myxoma virus, it is also a member of the Poxviridae family and is transmitted by an arthropod vector. Unlike with myxoma virus, lesions resolve spontaneously and treatment is usually not necessary. A predisposition of fibroma virus for cottontail rabbits is reported. Differentiation of this virus from myxoma virus is important because the prognoses for survival are significantly different.

Formation of a conjunctival membrane over the corneal surface is a condition unique to rabbits. This condition has been labeled pseudopterygium, corneal occlusion syndrome, conjunctival centripetalization, and epicorneal membrane (Figure 20-4). Progressive ingrowth of the bulbar conjunctiva occurs symmetrically and centripetally. The conjunctiva does not adhere to the corneal surface, separating this condition from true pterygium described in humans. The disease may be unilateral or bilateral. The cause has not been determined, although a collagen dysplasia has been proposed. Surgical correction is completed through a modified Arlt procedure. The conjunctival tissue is partially trimmed by sharp dissection, divided in half along the horizontal axis, and the leading edge is sutured to the conjunctival fornix. Because of the likelihood that this disease is immune mediated, application of cyclosporine, mitomycin C, or a steroid may decrease recurrence. However, topical administration of these agents may result in systemic immunosuppression and therefore they must be used with caution.

Figure 20-4 Pseudopterygium in a rabbit. The conjunctiva has grown centripetally over the corneal surface. Only a small area of cornea is noticeable (black ovoid area).

Nasolacrimal Disease

The tortuous path of the rabbit nasolacrimal duct predisposes it to recurrent dacryocystitis. Primary duct occlusion may occur with oil droplets or inspissated purulent material. Dental disease or osseous changes to the maxillary bone secondary to nutritional hyperparathyroidism may also lead to the development of duct obstruction. Of these, dental disease is alleged to be the most common cause. Malocclusion of the molars and premolars and, less frequently, the incisors results in retropulsion of the tooth and impingement on the nasolacrimal duct. Secondary infection ensues, and a wide range of organisms has been cultured, including Neisseria, Moraxella, Bordetella, Streptococcus viridans, Oligella urethralis, Pasteurella, and Pseudomonas. Clinical signs include epiphora, usually in conjunction with mucopurulent discharge. Secondary conjunctivitis may also be present. Dacryocystitis can be differentiated from primary conjunctivitis by digital pressure on the lacrimal sac. With dacryocystitis, a mucopurulent exudate can usually be expressed from the lacrimal puncta. Diagnosis is made on the basis of clinical signs and a negative fluorescein dye passage test result. A CT scan or plain radiograph of the head, sometimes augmented by dacryocystorhinography, may aid in differentiating the underlying cause and location of duct obstruction. Treatment is first aimed at correcting the underlying abnormality, especially correction of any dental disease (occlusal adjustment). The duct is then flushed with sterile saline through a 23-gauge lacrimal cannula. After flushing with saline, dilute povidone-iodine solution (1:50) is flushed through the duct. Repeated flushings may be necessary to maintain patency of the duct. If the duct cannot be flushed, long-term systemic antibiotic therapy (enrofloxacin 5mg/kg/day) may be necessary to control infection. Recurrences are common.

As in dogs, prolapse of the gland of the third eyelid may occur in rabbits. This is uncommon and usually involves the harderian gland. Chronic conjunctivitis commonly persists without treatment. Surgical therapy is curative and involves performing a modified Morgan-pocket technique. The gland should not be surgically excised because there is significant vascularization of the gland, so severe hemorrhage may occur.

Corneal Disease

The large, prominent globes and decreased blink rate of rabbits may predispose them to corneal disease. Corneal ulceration is common; it may be associated with trauma, exposure after anesthesia, distichiasis, entropion, and trichiasis and may occur secondary to blepharoconjunctivitis or dacryocystitis. Thorough examination will aid in differentiating the underlying cause. If no conformational abnormality is noted, trauma can be assumed. Diagnosis is facilitated by the use of fluorescein stain as in other species. Uncomplicated defects are treated symptomatically with a broad-spectrum topical antibiotic, such as chloramphenicol, several times daily. Ulcers that do not heal, have significant stromal loss, or are infected are deemed “complicated” and require more intensive therapy. Nonhealing or indolent corneal ulcers are common and should be treated like those in dogs. Aggressive corneal débridement with a cotton-tipped applicator after topical anesthesia is recommended. A grid or multiple superficial punctate keratotomy may also be necessary to promote healing. Cytology and culture and sensitivity testing of infected corneal ulcers are recommended so that appropriate antibiotic therapy can be initiated. When there is significant stromal loss or a descemetocele is present, referral to an ophthalmologist is warranted. Placement of a conjunctival pedicle graft is the treatment of choice, although this procedure is more difficult in rabbits owing to their notably thin cornea (0.36mm) compared with dogs (0.56mm). After surgery, antimicrobial therapy is initiated on the basis of cytology and culture results. Reflex uveitis secondary to keratitis likely occurs in rabbits as it does in dogs, and application of atropine may help alleviate ciliary spasm associated with uveitis through cycloplegia. However, the presence of atropinase in the rabbit uvea may prevent its effectiveness. Because atropinase is not universally present and not all rabbits are immune to atropine’s effects, its application is recommended. During treatment of corneal disease in rabbits, ophthalmic solutions or suspensions are preferred to ointments because of their normal grooming behaviors.

White corneal opacities are occasionally observed and may represent either mineral or lipid. Corneal dystrophy with subepithelial mineral deposition has been described as an inherited trait in American Dutch belted rabbits. Treatment is not usually necessary because the lesions do not cause visual deficits or keratitis. Corneal lipidosis occurs secondary to high cholesterol diets in most rabbit species. A hereditary hyperlipidemia has been described in the Watanabe rabbit. Lipid accumulates first at the limbus and then may proceed axially, resulting in either a subtle or marked opacity with obvious keratitis. Depending on the degree of keratitis and size of the plaque, conservative (dietary) therapy may be sufficient. However, if the plaque is large and causing visual deficits, a superficial keratectomy is recommended. Definitive diagnosis is obtained through histopathologic analysis of keratectomy specimens with appropriate stains such as oil red O.

Cataract

Cataracts may occur spontaneously or may be secondary to uveitis in rabbits. Some spontaneous cataracts (Figure 20-5) are suspected to be inherited in nature, although no genetic evidence is available because of the low incidence. Evaluation of laboratory New Zealand white rabbits revealed a 4% prevalence of spontaneous cataracts with no difference between males and females. Treatment is necessary only if secondary lens-induced uveitis or visual deficits are present. Removal of the lens via phacoemulsification is the treatment of choice. The procedure is similar to that performed in dogs, although the surgeon must take care upon entering the anterior chamber, because it is shallow and iris prolapse through the incision is more likely. Additionally, meticulous irrigation/aspiration of the peripheral lens cortex is necessary owing to the greater likelihood of lens fiber regrowth.

Figure 20-5 A complete, spontaneous cataract in a rabbit.

Uveitis was considered the most common cause of cataracts in rabbits. Rabbits were usually presented with a discrete, white, raised abscess within the iris overlying a focal cataract. Aqueous flare and hypotony were also present. Septicemia secondary to Pasteurella or Staphylococcus spp. was implicated as the cause of uveitis. Diagnosis was based solely on ophthalmic clinical signs, although many animals also had systemic disease consistent with septicemia. Diagnostic samples for culture and cytology via aqueocentesis were obtained infrequently due to the relative invasiveness of this procedure. When performed, organisms were rarely cultured or observed on cytologic preparations. Further evaluation of these iridal abscesses has revealed pyogranulomatous inflammation associated with lens capsule rupture (phacoclastic uveitis). Therefore the uveitis may have not been the inciting cause but the result of cataract formation with subsequent lens capsule rupture.

Intralenticular organisms have been identified in approximately 75% of rabbits with cataract formation with secondary phacoclastic uveitis. These organisms were 1 to 6mm in size and consistent with the obligate intracellular protozoa, Encephalitozoon cuniculi. Rabbits are infected with E. cuniculi after ingestion of food contaminated with urine. Nonocular signs include neurologic disease (head tilt, torticollis, seizures, ataxia, paralysis) and renal disease. Lens infection occurs in utero owing to vertical transmission from an infected dam. Dwarf and young rabbits are predisposed. Clinical signs are usually unilateral and include spontaneous lens capsule rupture with resultant phacoclastic uveitis (including aqueous flare, hypopyon, and hypotony), iridal granuloma formation, and cataract formation (Figures 20-6 and 20-7). Diagnosis is based on clinical signs along with supportive results from serology (indirect fluorescent antibody test, enzyme-linked immunosorbent assay) or PCR analysis of lens tissue. Serology is quite sensitive, as rabbits mount a humoral response within 2 weeks, and in one study 100% of rabbits with ocular signs were seropositive.

Figure 20-6 Focal lens capsule rupture, cataract, and iridal granuloma formation in a dwarf rabbit with Encephalitozoon cuniculi.

Figure 20-7 Same rabbit as in Figure 20-6, after 2 weeks without therapy. Phacoclastic uveitis is present as evidenced by lens capsule rupture, cataract formation, hyphema, and hypopyon.

Surgical therapy is recommended for E. cuniculi–induced lens capsule rupture and, when successful, is curative. The lens is removed by phacoemulsification and the iridal granuloma can be aspirated by automated irrigation/aspiration. Medical therapy alone may slow progression of the uveitis but rarely clears the infection. Medical treatment involves frequent use of topical antiinflammatory agents. Because of their relative lack of potential side effects, nonsteroidal antiinflammatory drugs (NSAIDs), such as flurbiprofen and diclofenac, are preferred over topical steroids. The antiparasitic agent albendazole has demonstrated efficacy in vitro, but its in vivo activity seems poor. The recommended dose of albendazole is 20 to 30mg/kg once daily for 3 to 10 days, and that for fenbendazole is 20mg/kg once daily for 28 days. However, they must be used with extreme caution because severe side effects, including death, have occurred with their use.

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