Etiopathogenesis of Uveitis

Uveitis can occur independently of disease in other ocular structures, or it can occur secondary to lens, corneal, or scleral disease. Additionally, uveitis can be associated with primary ocular disease or be secondary to neoplastic, infectious, or immune‐mediated diseases. Elucidating the etiology of uveitis in the dog can be difficult. However, because uveitis can lead to blindness or be a sign of a potentially fatal disease, attempting to define the etiology is always warranted. Uveitis should be approached in a systematic fashion evaluating for the most common diseases based on signalment, historical information including travel, ocular and physical examination findings, and locale.

Many etiologies for uveitis exist in all animal species. Most simply, causes can be divided into endogenous and exogenous. Endogenous causes originate from within the eye or spread to the eye from the bloodstream or from contiguous structures. Endogenous causes account for most cases of uveitis and include infectious, neoplastic, toxic, metabolic, and autoimmune diseases. Immune‐mediated and autoimmune disease is the most rapidly growing group of diseases responsible for endogenous uveitis. Trauma also includes surgical procedures and both perforating and nonperforating injuries with or without secondary infection. The more commonly recognized causes of uveitis in the dog are listed in Box 11.1.

General Uveal Inflammatory Responses

Several unique aspects of uveal inflammation include (i) the blood–aqueous barrier, (ii) the concentration of ascorbic acid and other antioxidants in the aqueous humor, (iii) the anterior chamber‐associated immune deviation, and (iv) the lack of an intrinsic lymphatic system.

The blood–ocular barrier is composed of the blood–aqueous barrier anteriorly and the blood–retinal barrier posteriorly. Morphologically, this barrier consists of tight junctions (zonulae occludens) between nonpigmented ciliary body epithelial cells, tight junctions and gap junctions in the iris vascular endothelium, and nonfenestrated impermeable capillaries in the iris. Evolutionary divergence in ocular defense mechanisms has resulted in extreme differences of blood–aqueous barrier stability among different mammalian species. Destabilization of the blood–aqueous barrier marks the onset of anterior uveitis.

Chemical Mediators of Inflammation

Much effort has been directed toward identifying the chemical mediators of ocular inflammation because their recognition has direct therapeutic implications. While progress is always being made toward understanding inflammation, the variations in species’ responses to inflammation and the varying diseases among species slow the progress. Invasive investigative methods can also affect ocular inflammations, and hamper serial methodologies.

PGs are the most widely studied mediators of ocular inflammation and are considered to be primary mediators of ocular inflammation. Cyclooxygenase has been identified in all cell types, except for mature red blood cells, and PGs are produced by the irides of all species studied to date. The most notable pathological ocular effects of PGs include miosis, hyperemia, changes in vascular permeability, and alterations in intraocular pressure (IOP) depending on the particular PG and species in question.

Arachidonic acid derivatives also appear to play a key role in ocular inflammation. Arachidonic acid is released from damaged cellular membranes through phospholipases acting on cellular phospholipids. It can then enter one of at least three metabolic pathways: the cyclooxygenase, lipoxygenase, or oxidation pathway. The cyclooxygenase pathway produces PGs, thromboxane, and prostacyclin, and the lipoxygenase pathway produces leukotrienes, hydroperoxyeicosatetraenoic acid, and hydroxyeicosatetraenoic acid.

Leukotrienes are synthesized in the cornea, conjunctiva, anterior uvea, and lens. Species variations exist in the extent and duration of leukotriene production. Leukotrienes are potent vasoactive substances and chemoattractants. Their chemotactic, humoral, and cellular activities are greater than those of PGs.

Substance P, a unadecapeptide normally present in sensory nerves, may be important in uveitis, particularly when associated with corneal irritation. Ulcerative keratitis causes varying degrees of uveitis, but it does so through a poorly understood “axonal reflex.” With corneal irritation, antidromic impulses mediated by the trigeminal nerve (ophthalmic branch) reaching the iris and ciliary body are believed to stimulate release of substance P. This causes vascular dilatation and altered permeability as well as PMN chemotaxis.

Numerous other chemical mediators also have contributory, albeit largely undefined, roles in ocular inflammation. Histamine is important in the initiation of many inflammatory processes, and its release from mast cells leads to an increase in vascular permeability, but histamine’s role in canine uveal disease is poorly understood. Reactive oxygen metabolites, angiotensin‐converting enzyme, and basic fibroblast growth factor may also play a role in uveitis

Clinical Manifestations and Diagnosis

The clinical signs of anterior uveitis can be for uveitis, such as aqueous flare and hypopyon, while others are general ocular responses, such as blepharospasm and ocular hyperemia. Anterior uveitis can also be a secondary component of other ocular diseases, such as corneal ulceration and glaucoma, demonstrating the need for a complete ophthalmic examination. The clinical signs of uveitis are listed in Table 11.1.

Excessive lacrimation, blepharospasm, and photophobia are readily observed. These signs suggest varying degrees of ocular discomfort not specific to uveitis. Acute uveitis tends to be more painful than chronic uveitis. The pain is referred to the ocular and periorbital regions. Pain and photophobia are caused by ciliary spasm. Excessive lacrimation is thought to occur secondary to the photophobia.

Ciliary flush is hyperemia of the deep, perilimbal, or circumcorneal anterior ciliary vessels and is common with deep corneal and intraocular disease (i.e., uveitis and glaucoma). Congestion of the conjunctival vessels also commonly occurs with uveitis, and in severe cases, uveitis can even lead to chemosis. Determination of the presence of ciliary flush is important for diagnostic purposes because it must be distinguished from superficial conjunctival hyperemia, which is commonly seen with extraocular disease such as allergic conjunctivitis. Distinguishing between these vascular patterns may be facilitated by topical application of a sympathomimetic agent (e.g., 1% epinephrine solution). The topical sympathomimetic agent will have a greater immediate vasoconstrictive effect on the superficial conjunctival vessels than on the deeper anterior ciliary vessels. In addition, conjunctival vessels are noted to move on the surface of the globe, whereas the anterior ciliary vessels remain stationary within the sclera during movement of the globe.

Corneal edema with an associated increase in corneal thickness develops with anterior uveitis secondary to both an increase in endothelial permeability and a decrease in Na/K‐ATPase pump site density (Figure 11.6). Severe edema may result in painful bulla formation. Morphologically, edematous endothelial cells with disrupted intercellular junctions and a normal cell density are seen. Persistent corneal edema may be followed by peripheral corneal vascularization. Pupillary constriction, or miosis, is a very common sign of anterior uveitis. Miosis occurs in response to PGF₂ acting directly on the iris sphincter muscle. Inflammatory mediators also cause painful spasm of the ciliary body musculature, causing what is described as “brow ache” in humans. Subtle miosis is often more apparent when examining both eyes simultaneously in a darkened room using retroillumination with a penlight or Finoff transilluminator. Iris swelling from edema and cellular infiltrates may also, in conjunction with inflammatory mediators, impede normal pupil mobility. Subclinical uveitis often manifests with a pupil that dilates more slowly after short‐acting mydriatic therapy (i.e., 1% tropicamide) compared with the normal eye.

Synechiae formation is one of the more serious complications of anterior uveitis, and it results from inflammatory cells, fibrin, and fibroblasts leading to adhesions of the iris to the lens or peripheral cornea (Figure 11.7). Three types of synechiae can develop; they include (i) anterior synechia (iris–posterior cornea); (ii) posterior synechia (iris–anterior capsule of the lens); and (iii) peripheral anterior synechia (between the basal iris and ciliary body involving the opening of the ciliary cleft). Peripheral anterior synechiae form because of shallowing of the anterior chamber and the iridocorneal cleft as a result of pupillary block, secondary to organization of inflammatory exudates in the angle with gradual attraction of the iris toward the angle structures, and with intense swelling of the root of the iris. Posterior synechiae are a consequence of the central portion of the anterior lens capsule extending more anteriorly than the peripheral lens. With miosis, the iris is in more intimate contact with the lens, increasing the surface area for synechia formation. Posterior synechia can cause occlusion of the pupil, leading to loss of sight or seclusion of the pupil, and resulting in iris bombé with subsequent acute glaucoma (Figure 11.8). Synechia can result in a fixed miotic or midrange pupil. With chronic synechiae, pigment often migrates from the surface of the iris onto the anterior lens capsule, which is more likely to interfere with vision if the pupil is miotic.

Aqueous flare, increased turbidity of aqueous humor, occurs as protein‐rich aqueous humor and cellular components accumulate within the anterior chamber after the blood–aqueous barrier has been disrupted. Aqueous flare is visualized when light scattering from particles suspended in the anterior chamber causes a continuous light reflection throughout the chamber. This continuous beam effect is called the Tyndall phenomenon, and it is analogous to shining a flashlight within a smoke‐filled room. Observation of the Tyndall phenomenon is indicative of aqueous flare, and aqueous flare is pathognomonic of the breakdown in the blood–aqueous barrier for anterior uveitis. Varying degrees of aqueous flare are possible, and though this scheme is highly subjective, some clinicians attempt to quantitate flare numerically as 1+ to 4+, with higher numerals indicating increased severity. The term fibrinous (or plasmoid) aqueous refers to aqueous humor that has an increased level of aqueous protein approximating that of normal plasma. This condition occurs most commonly in cases of acute, severe anterior uveitis with sudden onset. Lipid‐laden aqueous is also possible if the patient has concurrent hyperlipidemia in which the aqueous assumes a milky‐white appearance (Figure 11.9).

Cells from the inflammatory process pass into the aqueous humor either from diffusion or from active migration from the uvea. They either are manufactured locally or egress through the capillary walls from the blood into the uveal tissue and into the aqueous humor. Keratic precipitates (KPs) are accumulations of inflammatory cells, fibrin, and pigment from the iris that are deposited on the corneal endothelium. KPs are usually located inferiorly on the cornea in a triangular shape with the apex located superiorly. Convection currents in the anterior chamber cause the aqueous humor to rise along the warm dorsal iris, and fall along the cooler dorsal and central cornea creating its characteristic formation. It is important to note KPs because their presence is always indicative of active or previous uveitis.

The deposition of red and white blood cells within the anterior chamber are the most marked examples of blood–uveal barrier breakdown and are termed hyphema and hypopyon, respectively (Figure 11.10). In both instances, cellular components typically gravitate toward the ventral anterior chamber and settle in a homogeneous layer. If bleeding was initially extensive or is continuous, complete (i.e., total) hyphema with filling of the entire anterior chamber may occur. Layering in the hyphema may indicate rebleeding. Occasionally, iridal hemorrhage may be seen. Hypopyon rarely occupies more than a third of the anterior chamber and is easily missed because the ventral anterior chamber is often obscured by the third eyelid (Figure 11.11). Generally, hypopyon leaves the eye rapidly through the trabecular meshwork when treatment of the inflammatory processes is initiated and effective.

Cytological evaluation of aqueous humor, bacterial or fungal culture of the aqueous, vitreous aspirates, or a combination thereof may be beneficial in determining the cause of uveitis. Aqueous aspiration appears to yield useful and positive results, mainly in eyes with visible exudates or in animals suspected of having lymphosarcoma. Most commonly, aqueous aspiration yields nonspecific inflammatory cells. Because of the rarity of specific results and the exacerbation of existing uveitis, the procedure is not recommended in most cases. In patients with concurrent posterior uveal involvement, vitreous aspiration is more likely to yield positive results than aqueocentesis (see Chapter 13).

Preiridal fibrovascular membranes (PIFMs) arise from the anterior border layer of the iris and develop secondary to chronic ocular disease such as uveitis, glaucoma, intraocular neoplasia, endophthalmitis, and retinal detachment. The clinical term for this condition is rubeosis iridis. Clinically, a haphazard array of very small vessels is seen on the iridal surface (Figure 11.12). PIFMs are always preceded by ocular disease, and their development can lead to hyphema because of the fragility of the vessel walls and to glaucoma because of membrane formation within and over the iridocorneal angle. In addition to rubeosis iridis, diffuse iris hyperpigmentation can occur with chronic anterior uveitis. This condition is more obvious in eyes with lightly pigmented irides and in cats.

Decreased IOP is one of the earliest and most subtle indications of uveitis. Proposed mechanisms for decreased IOP include both decreased aqueous humor production with breakdown of the blood–aqueous barrier and increased uveoscleral flow mediated in part by PGs. IOP will vary depending on the duration and severity of uveitis. In acute or subacute uveitis, IOP is usually decreased for the previously mentioned reasons; in chronic uveitis, fibrosis or atrophy (or both) of the ciliary body may contribute to decreased secretory function with subsequent ocular hypotony. Marked ciliary body dysfunction and hypotony may result in phthisis bulbi.

Secondary glaucoma is a common manifestation of severe or protracted uveitis. The causes of secondary glaucoma include obstruction of the angle by inflammatory debris, iris bombé that occurs with formation of annular posterior synechiae, extensive anterior peripheral synechia, and formation of PIFMs. An IOP of less than 10 mmHg is consistent with uveitis. Cataracts, especially anterior subcapsular cataracts, occur commonly with chronic anterior uveitis. They are thought to arise from inflammatory mediators in the aqueous humor interfering with normal lens metabolism. Lenticular changes are not specific and include epithelial metaplasia or posterior migration and liquefaction, degeneration, or necrosis of lens fibers. Posterior synechiae can also result in cataract formation.

Systemic Evaluation

When the diagnosis of uveitis is made, an attempt should be made to identify the etiology. Some causes are readily apparent, such as when anterior uveitis occurs in conjunction with a hypermature cataract. Conversely, extensive diagnostic testing and evaluation frequently do not lead to a specific conclusion. A complete ophthalmic and physical examination is always indicated when a diagnosis of uveitis has been made. Physical examination should include evaluation of the skin, looking for depigmented areas or draining lesions, lymph node palpation, auscultation, and abdominal and possibly rectal (especially in intact male dogs) palpation. A complete blood count and serum panel is usually indicated. Selected titers are run based on the endemic diseases in the dog’s location and in areas where the dog may have traveled. Thoracic radiographs are also considered part of the minimal screening protocol when systemic disease is suspected. Radiographs are evaluated for evidence of metastatic or fungal diseases. Additional serological tests and diagnostics are indicated according to the clinician’s index of suspicion. Refer to the section on selected uveal diseases in this chapter as well as to Chapter 19 for further discussion.

Therapy for Anterior Uveitis

Topical anti‐inflammatory therapy should be instituted immediately after the diagnosis of anterior uveitis is made, even in those patients with suspected systemic disease. Topical therapy alone may suffice for mild anterior uveitis, but for severe anterior uveitis, posterior uveitis, and systemic disease, systemic therapy as dictated by the primary disease is also indicated (Table 11.2).

Lens‐Induced Uveitis

LIU is a common complication of cataract formation in the dog (also see Chapter 12). Historically, LIU was associated with hypermature cataracts, but studies using fluorophotometry, laser flaremetry, and applanation tonometry have shown that dogs with all stages of cataracts have evidence of at least subclinical uveitis. Most likely, small amounts of lens protein escape the normal lens and induce T‐cell tolerance. Increased immune system exposure to lens crystallins by lens trauma, spontaneous lens resorption, or cataract extraction may overwhelm this tolerance and induce an intraocular or systemic cell‐mediated and/or humoral immune response. Two distinct types of LIU are recognized in the dog. Phacolytic uveitis occurs in dogs with rapidly developing or hypermature cataracts in which soluble lens protein leaks through an intact lens capsule. This type of LIU is nongranulomatous and is characterized by mild lymphocytic–plasmacytic uveitis, not unlike that occurring with most idiopathic uveitides. The diagnosis of this type of LIU is presumptive, being made on the observation of cataracts and the absence of other ocular or systemic disease. Phacolytic LIU may develop more rapidly in young dogs after the onset of cataract. Long‐term success rates of cataract surgery in dogs with LIU may be lower than in dogs without LIU. LIU also needs to be treated in dogs that are not cataract surgical candidates because the uveitis is painful and treatment may delay the onset of secondary glaucoma. Granulomatous LIU also occurs in dogs with an intact lens capsule but usually occurs in older dogs with rapidly progressing cataracts, especially Miniature Schnauzers, or long‐standing cataracts. These eyes have severe uveitis, often with large KPs, and are less responsive to therapy.

The other type of LIU in dogs is phacoclastic uveitis that occurs after lens capsule rupture, which causes sudden exposure of intact lens protein in large amounts sufficient to overwhelm the normal low‐dose T‐cell tolerance to lens proteins. There may be a history of recent ocular trauma; however, lens penetration is rarely suspected. Clinically, there is evidence of corneal penetration, varying degrees of anterior uveitis, and exudate or hemorrhage in the anterior chamber. Usually, the corneal wound has sealed and the anterior chamber has reformed.

Lensectomy using phacoemulsification is the ideal therapy for lens rupture in the dog. One study showed that the average number of days to referral in cases amenable to surgery was 3 versus 10 in dogs that were not considered surgical candidates. Medical therapy was not successful in dogs with ruptured lenses, and most of those eyes developed phthisis bulbi or required enucleation because of progressive anterior uveitis and secondary glaucoma.

Anterior Uveitis Secondary to Corneal and Scleral Disease

Anterior uveitis occurs commonly secondary to corneal ulceration. Miosis is the most common clinical sign of anterior uveitis seen in dogs with corneal ulceration, but decreased IOP and aqueous flare are also seen.

Non‐necrotizing scleritis in dogs is relatively common and does not typically involve the anterior and posterior segments of the eye. Necrotizing scleritis, however, may cause anterior uveitis, vitritis, subretinal masses, tapetal degeneration, hemorrhage, and edema. Therapy with immunosuppressive dosages of prednisone and azathioprine is indicated but may not be effective in the low term.

Uveodermatologic Syndrome

UDS, or Vogt–Koyanagi–Harada (VKH)‐like syndrome, is a disease of dogs that causes anterior uveitis, chorioretinitis, poliosis, and vitiligo. The syndrome in dogs was initially termed VKH‐like syndrome because of similarities to a disease in humans known as VKH syndrome, but the term UDS has also been adopted to further separate the disease in dogs from that in humans because of the absence of neurological signs in dogs. The disease was first reported in Japan in 1977. The pathogenesis of UDS is not completely understood. VKH syndrome in humans is an autoimmune disease directed against melanocytes and is mainly mediated by cellular immune responses. Experimentally, Akita dogs have been immunized with tyrosinase‐related protein, an enzyme involved in melanin formation that is expressed specifically in melanocytes. The Akitas developed some clinical and histological signs consistent with UDS, supporting the similarities between the canine and human diseases. UDS appears to affect primarily young adult dogs; the mean age from two reports was three years. UDS also appears to occur more frequently in the Akita, Samoyed, Siberian Husky, and Shetland Sheepdog than in other breeds, but many other breeds can be affected.

Ocular findings include bilateral progressive anterior uveitis or panuveitis, iris or choroidal depigmentation, bullous retinal detachment, and blindness. Cataract, extensive posterior synechiae, iris bombé, and secondary glaucoma with buphthalmos occur with chronicity in a high percentage of affected dogs. Dermatological changes usually follow the development of ocular disease, and include vitiligo of the facial mucocutaneous junctions, nasal planum, scrotum, and footpads; however, generalized vitiligo may occur (Figure 11.13). Poliosis may be confined to the facial region or be generalized. Alopecia occurs inconsistently. General physical examination on affected dogs is normal, excluding the dermal and ocular changes.

Routine laboratory parameters are normal. Immune function tests and titers for multiple infectious diseases have been negative. Histopathologically, the primary ocular change is a granulomatous panuveitis with prominent perivascular lymphoid aggregates and melanophages. Retinal detachment, destruction of the retinal pigmented epitheliae, subretinal neovascularization, choroidal scarring, and signs consistent with secondary glaucoma are also seen frequently.

Immunosuppressive drugs are the mainstay of therapy. Standard therapy for anterior uveitis with topical steroids and atropine (if the IOP is not elevated) is initiated. Oral prednisone at immunosuppressive doses is also used. Subconjunctival injections of steroids, such as methylprednisolone, are used by some clinicians. Generally, there is a relatively rapid response to therapy. Unfortunately, many dogs have recurrence of clinical signs if the dose of oral prednisone is decreased but have the undesirable side effects of weight gain, polyuria, and polydipsia if they are continued. Therefore, other immunosuppressive drugs, such as azothioprine, are often combined with corticosteroids in the long‐term management of UDS.

Mycoses‐Associated Uveitis

Disseminated mycotic infections with ocular involvement are relatively common among dogs living in endemic areas. Even though mycotic infections typically involve multiple body systems, ocular disease is often the reason for presentation. Common systemic mycoses include blastomycosis, coccidioidomycosis, histoplasmosis, and cryptococcosis (Table 11.3). Less frequently occurring infections are aspergillosis and candidiasis. Inhalation is believed to be the primary route of infection for all the major systemic mycoses, with later hematogenous spread to the eye. Direct animal‐to‐animal or animal‐to‐human infection is rare. Ocular involvement may be unilateral or bilateral, and infections of the paranasal sinus, orbit, and optic nerve may affect the eye secondarily.

The diagnosis is made on the basis of concurrent clinical signs, which vary between mycotic organisms; identification of organisms in ocular or other tissue aspirates; or the results of fungal culture, histopathological examination, or various serological tests.The preferred systemic therapy for each type of mycosis varies. Eyes that are potentially visual should be treated topically with corticosteroids and atropine if hypotensive or normotensive, but a painful, blind eye is best enucleated

Parasitic Diseases

Protozoal Diseases

Rickettsial Diseases

Viral Diseases

Bacterial Disease

Brucella canis is an aerobic, Gram‐negative coccobacillus that can survive in mononuclear cells. Infection is by penetration of the organisms through mucous membranes of the oropharynx, genital tract, and conjunctiva. The concentration of the organism is highest in semen and vaginal discharge in infected dogs. Abortion and infertility are common clinical signs that occur in breeding dogs, but neutered dogs may also be affected. Ocular signs occur in ~14% of dogs with brucellosis. The more common ocular findings include endophthalmitis, chronic uveitis, hyphema, and chorioretinitis. Diagnosis is made using the slide agglutination test in combination with the agar gel immunodiffusion assay (AGID) or by positive culture. Antimicrobial therapy is complicated and must be continued in the long term because of the intracellular nature of the organism, but successful treatment has been reported.

Leptospirosis is caused by a spirochete, a filamentous bacterium belonging to the genus Leptospira, which includes many species and serovars. Leptospira organisms are most commonly transmitted through urine. Vasculitis and endotheliitis involving the kidneys, liver, spleen, muscles, CNS, and eyes occur. Ocular lesions are infrequently seen but may include anterior uveitis. The leptospira organisms may be cultured from the aqueous humor of some dogs.

Algal Disease

Prototheca zopfii and Prototheca wickerhamii are algae that lack chlorophyll and are known pathogens in dogs and other animals. The primary clinical sign is usually hemorrhagic diarrhea; however, dogs may present with blindness as the initial sign. Neurological signs may also occur, and ocular signs may include anterior uveitis, secondary glaucoma, chorioretinitis, and retinal detachment. Cytology or culture of vitreal aspirates may be diagnostic. Prototheca sp. are extracellular, round to oval organisms with thin, unstained walls. Larger cells may contain endospores. Therapy with itraconazole has been attempted but has been unsuccessful in the long term.

Hyperlipidemia

Dogs with hyperlipidemia resulting from elevations in either cholesterol or triglycerides may have associated ocular abnormalities. Lipid‐laden aqueous humor was discussed briefly in the “Uveal Inflammation” section as occasionally occurring with anterior uveitis (see Figure 11.9). Lipoproteins of dogs range in size from 50 to 350 Å in diameter. However, the iridal vascular endothelium and nonpigmented ciliary body epithelium normally prevent particles greater than 40 Å from entering the aqueous humor. Breakdown of the blood–aqueous barrier (i.e., anterior uveitis) concurrent with hyperlipidemia can result in lipid‐laden aqueous.

Additional ocular manifestations of hyperlipidemia may include lipid engorgement of retinal vasculature and infiltration of the perilimbal cornea, conditions referred to as lipemia retinalis and corneal lipidosis (or arcus lipoides corneae), respectively. Lipid‐laden aqueous and lipemia retinalis are likely to resolve with resolution of the primary disorder.

Pigmentary and Cystic Glaucoma (Pigmentary Uveitis)

Uveal cysts are usually considered to be benign; however, reports describing an association with cysts and glaucoma in both the Golden Retriever and the Great Dane have emerged. A syndrome that occurs primarily in Golden Retrievers in the United States has been referred to as both pigmentary uveitis and pigmentary and cystic glaucoma. Pigment dispersion on the anterior lens capsule in a radial orientation is the most frequently observed early clinical sign (Figures 11.14 and 11.15). Other clinical signs include uveal cysts, spiderweb‐like fibrinous debris in the anterior chamber, cataracts, and posterior synechiae. Secondary glaucoma occurs within in a few months in the majority of eyes, and this disease is usually bilateral.

The syndrome in Great Danes may not be identical to that in the Golden Retrievers. Consistent findings in Great Danes with ciliary body cysts include multiple cysts in the anterior and posterior chambers and glaucoma. The cysts are variable in size, very poorly pigmented, and usually transparent. The entire posterior chamber is filled with cysts that may push the iris forward.

Solid Intraocular Xanthogranuloma in Miniature Schnauzer Dogs

Solid intraocular xanthogranulomas were identified in four globes from three older Miniature Schnauzers that all had a history of diabetes mellitus, hyperlipidemia, and bilaterally severe uveitis with glaucoma that was believed to be lens‐induced. Grossly, all globes were filled with a heterogeneous tan mass.

Hyperviscosity Syndrome

Monoclonal gammopathy associated with lymphoproliferative disorders may result in HVS. HVS causes clinical signs referable to multiple organ systems, including the cardiac, renal, hemostatic, ocular, and central nervous systems. In the dog, HVS associated with increased serum concentrations of IgG, IgM, and IgA is reported. HVS secondary to polycythemia vera has also been reported. Anterior segment findings include conjunctival hyperemia, corneal edema, hyphema, and secondary glaucoma, all of which are likely related to concurrent anterior uveitis. Posterior segment may include retinal vascular dilatation, tortuosity, microaneurysms, retinal hemorrhage, retinal detachment, chorioretinitis, and papilledema.

Sulfonamide Hypersensitivity

Multiple clinical abnormalities have been described in dogs with sulfonamide hypersensitivity. General signs include fever, arthropathy, blood dyscrasias, glomerulonephropathy, hepatopathy, skin eruption, retinitis, and keratoconjunctivitis sicca. Uveitis may also occur alone or secondary to intraocular bleeding from thrombocytopenia.

Emergency Management of Acute Ocular Trauma

Cases of acute ocular trauma must be handled on an emergency basis. When a dog is presented with ocular trauma, the dog should be restrained or sedated as needed to facilitate an ocular examination. If possible, the clinician should determine whether a laceration or rupture of the globe is present. Assessment of the extent of globe laceration or rupture is not always easy, but it is important as a prognostic indicator. If the globe is ruptured, further examination to assess the degree of rupture and foreign body examination should be delayed until the animal has been anesthetized (Box 11.2).

Ancillary Diagnostic Procedures

Following a thorough ocular examination, additional diagnostics may be required. Radiography of the skull, including oblique views of the orbit or orbits, will confirm or rule out the presence of fractures and establish whether gunshot injury is involved. B‐scan ultrasonography is specifically indicated when the normally transparent ocular media are opaque. Integrity of the lens and posterior sclera as well as the position of the lens and retina can generally be determined with B‐scan ultrasonography. Computed tomography (CT) and magnetic resonance imaging (MRI) may be beneficial in assessing trauma, especially when intraocular foreign bodies (IOFBs) are suspected. Care should be taken with MRI because metallic foreign bodies can incite additional damage.

Treatment of Blunt Injuries

Intense pressure exerted on the globe during blunt trauma may result in vector forces reflecting off the posterior sclera and transferring anteriorly, causing a blowout rupture of the perilimbal cornea or anterior sclera. Some causes of blunt injuries are impacts by golf balls and baseball bats; commonly, the owner is not aware that the dog is in such close proximity when the accident occurs.