10 The canine uveal tract is divided into anterior (iris and ciliary body) and posterior (choroid) portions. The anatomic divisions are also useful clinically, as often the anterior and posterior uvea are affected by separate clinical disorders. Heterochromia iridis indicates multiple colors within one iris or between the irides. In many breeds, a unilateral completely blue iris is acceptable for that breed standard; in other breeds a unilateral blue iris is rejected for registration. In some breeds, such as the Siberian Husky, both irides can be blue (Figure 10.1). Blue irides in certain breeds, such as the Dalmatian, have been associated with deafness and cardiac defects. The ocular fundus in eyes with blue irides can be subalbinoid with limited to no pigmentation of the nontapetal fundus visible with ophthalmoscopy. The tapetum lucidum is usually present, appearing as a yellow–green triangular area (the tapetal fundus), but is occasionally absent (atapetal). Figure 10.1 (A) Heterochromia iridis in a Siberian Husky. Many breed standards allow one or both eyes to be blue. (B) Heterochromia iridis is also associated with merling in the dog. Combinations of brown, blue, and white are common. Heterochromia iridis is also associated with the merling gene and coat color in many breeds. In heterozyzous dogs (Mn), heterochromia irides can appear as completely blue, or as partially brown with focal areas of blue and white. The ocular fundi in these dogs can be totally pigmented, subalbinoid with or without a tapetal fundus, and either pigmented or hypopigmented nontapetal fundus and a normal to markedly reduced tapetal fundus. In those merled breeds when the merling genes are homogyzous (MM), multiple ocular anomalies (merle ocular dysgenesis) occur with heterochromia iridis in puppies with excessively white hair coats (Figure 10.2; see also Figure 4.1). These abnormalities include microphthalmia, pupillary size and shape abnormalities, focal iridal hypoplasia and colobomas, cortical cataracts, equatorial staphylomas, retinal dysplasia and retinal detachments. Iris color is usually blue but occasionally yellow or very light brown. The ocular fundus is usually subalbinoid with a lightly pigmented nontapetal fundus, and either atapetal or a yellow–green tapetal fundus. Figure 10.2 (A) Heterochromia iridis is also associated with microphthalmia and other ocular anomalies in the homozygous merle (excessively white) dogs. This syndrome is termed merle ocular dysgenesis. Note the malformed pupil and unequal size globes in this Great Dane puppy. (B) Heterochromia iridis in an excessively white Australian Shepherd puppy with bilateral microphthalmia. The central iris is hypoplastic and contains some persistent pupillary membranes. Early cataract is present as well, noted as dark wisps within the lens viewed via retroillumination. Persistent pupillary membranes (PPMs) are the most frequent congenital defect of the canine anterior uvea (Figure 10.3; see also Figure 8.3). Pupil formation occurs in the last one‐third of gestation, but, not infrequently, pups at 12–14 days postnatal have some lingering pupillary “tags.” By 4 months or with maturation of the eye, any PPMs remaining are usually considered abnormal. Figure 10.3 (A) Persistent pupillary membrane (PPM) and secondary axial anterior capsular cataract in an Old English Sheepdog puppy with microphthalmia. Note the base of the PPMs is on the anterior surface of the iris (collarette region). (B) Rather large PPMs that are adherent to the posterior cornea. (C) Aniridia, the developmental absence of the iris, is illustrated here. PPMs are all that exist of the iris. The equator of the lens and the ciliary processes are visible. A nuclear cataract is present. Some remnants of the iris are usually present microscopically. PPMs usually originate from the collarette region on anterior surface of the iris; this is also the area of the minor arteriolar circle of the iris. PPMs appear as fibrous to pigmented bands of variable width which attach to other areas of the iris, the posterior surface of the cornea, and/or the anterior lens capsule. Those attaching to the cornea and the lens produce posterior corneal opacity and anterior capsular cataract, respectively. PPMs that connect to different areas of the iris cause pupillary shape abnormalities and irregular dilation. Progression of the corneal and lens opacities with PPMs is unlikely. Treatment is not usually necessary. Doppler ultrasound can be used to determine if PPMs have blood flow. Iridal nests or iridal arrests are punctate foci of pigmented tissues that reside on the central anterior lens capsule, the result of congenital deposition of cells during embryologic development and/or the formation of the pupil (variation of PPM) (Figure 10.4). They do not cause cataract formation. They are variable in size and number of pigmented cells, but do not adversely affect vision in the dog. Treatment is generally not required. If the dog’s day vision is impaired, drug‐induced mydriasis may improve vision. Figure 10.4 Large number of iridal nests or arrests on the central anterior lens capsule. They do not cause cataract formation. Colobomas are defects of congenital origin (Figure 10.5). Typical colobomas occur at the 6 o’clock position and atypical colobomas occur at any other position. Iridal colobomas affect heterochromic eyes more frequently, especially if the globe is microphthalmic and has other anomalies. Iridal hypoplasia is a congenital thinning of the iris tissue. Often, the tissue can be transilluminated revealing a reflection from the fundus. Figure 10.5 (A) Atypical iridal coloboma in a young Australian Shepherd puppy at the 9 o’clock position. The defect is nearly full‐thickness and partially exposes the posterior iridal pigmented epithelium. (B) Sector iridal hypoplasia in a puppy. The affected iris is a lighter brown and has distorted the pupil. The adjacent sclera is also malformed. (C) Iris hypoplasia in a young mixed‐breed dog. The defects in the iris at 9 o’clock position are not full‐thickness. The pigmented posterior epithelium can be visualized through the thin or absent iris stroma. Inflammations are the most frequent group of acquired diseases of the canine anterior uvea. These inflammations (anterior uveitis or iridocyclitis) are infectious (virus, bacterial, fungal, parasitic, other), traumatic, neoplastic, toxic, metabolic, or autoimmune in origin. The key clinical question is to separate those iridocyclitides associated with other eye diseases from those secondary to systemic diseases (which often affect both eyes). In addition, simultaneous involvement of the posterior uvea, the choroid, signals panuveitis and a more serious clinical disease involving the retina and optic nerve. The clinical signs of acute uveitis include photophobia, tearing or lacrimation, blepharospasm, eyelid edema, and a “red” eye (Figure 10.6). The ophthalmic examination findings include aqueous flare, ciliary flush and episcleral injection, conjunctival hyperemia, variable corneal edema, miosis, iris swelling, deep corneal vascularization, hypopyon, hyphema, keratic precipitates, and decreased intraocular pressure. When both eyes are involved and systemic disease is suspected, a complete blood count, serum biochemical profile, urine analysis, and chest and abdominal imaging are usually included in the initial workup. If the patient resides or has traveled to geographic locations with a high incidence of certain infectious diseases, specific testing for evidence of infection or exposure to these infectious agents (serology, polymerase chain reaction, etc.) is indicated as well. Figure 10.6 (A) Acute iridocyclitis of less than 24 hours’ duration. Note the conjunctival hyperemia, miosis, and profound corneal edema. (B) Acute iridocyclitis secondary to a central deep corneal ulcer. Note the swollen iris, hypopyon, and aqueous flare. The pupil has been dilated pharmacologically. (C) Ciliary flush in acute anterior uveitis represents hyperemia of the deep perilimbal or circumcorneal anterior ciliary vessels which are important indicators of intraocular inflammation. (D) Clotted fibrin in the anterior chamber of a dog following phacoemulsification of a hypermature cataract 5 days previously. (E) Lipemic aqueous in a dog with hyperlipoproteinemia. If blood lipid levels are elevated and the patient develops uveitis, lipid can leak into the eye and result in a milky color to the aqueous humor. This opacity is more dense than aqueous flare. In this case, the dog has a corneal ulcer (note fluorescein retention) and reflex anterior uveitis. The finding of lipemic aqueous should initiate a systemic workup. The treatment and prognosis of acute iridocyclitis depends on its cause and response to therapy. Treatment is directed at the suspected cause as well as nonspecific therapy for the anterior uveal inflammation. Pupillary dilation is important to reduce the chance of posterior synechiae and cataract formation, stabilize the blood–aqueous barrier, and decrease the pain associated with iridal and ciliary body musculature spasms. Atropine (1%) is recommended to effect (maximal mydriasis), but should not be instilled excessively as it significantly decreases tear production. Anti‐inflammatory agents including topical, systemic, and subconjunctival corticosteroids, as well as topical and systemic nonsteroidal agents, decrease the uveal inflammation, miosis, and pain. Topical and/or systemic antibiotics, and systemic antifungals, can be utilized when infectious disease is suspected. Chronic inflammations of the anterior uvea are less frequent than the acute forms, but are noted with increasing frequency in clinical practice, and generally lead to the development of serious complications, including synechiae formation, cataract formation, retinal degeneration and detachments, and glaucoma (iridocorneal closure and peripheral anterior synechiae formation, or pupillary occlusion/annular posterior synechiae/iris bombé), at high frequencies. The history is usually one of protracted anterior uveitis that responds only partially to intense or long‐term therapy. Some of the more common causes of chronic uveitis in the dog include cataract formation (usually cataract hypermaturity), systemic mycotic infections (blastomycosis, cryptococcosis, and coccidioidomycosis), uveodermatologic syndrome (mainly in the Arctic breeds), and other forms of autoimmune uveitis, Golden Retriever uveitis (pigmentary uveitis; see Figure 9.10), and neoplasia (either systemic or local) (Figure 10.7). Figure 10.7 (A) Uveodermatologic syndrome in an Atika during a remission phase. Aggressive systemic and topical corticosteroids and azathioprine have markedly reduced the uveitis. Note the pigment foci on the anterior lens capsule and mulitfocal posterior synechiae. (B) Chronic anterior uveitis has distorted and fixed the pupil with nearly complete posterior synechiae. A hypermature cataract has resulted from the chronic intraocular inflammation. The observations from the ophthalmic examination of eyes with chronic uveitis include those seen in acute iridocyclitis, as well as posterior synechia formation, irregular and fixed pupil, pigment deposits from the iris on the anterior lens capsule, cataract formation, either loss or hyperpigmentation of the iris, ectropion uvea (distortion or eversion of the pupillary iris revealing pigment from its posterior surface), decreased intraocular pressure (until secondary glaucoma develops), secondary glaucoma, and phthisis bulbus (atrophy of the globe). Inflammatory membranes can cross the pupil and adhere to the anterior lens capsule and extend onto the iridal surface (as preiridal fibrovascular membranes). Pupillary seclusion, usually from annular (360°) posterior synechiae formation, and formation of iris bombé lead to secondary glaucoma. The goals of therapy are to reduce the anterior uveal inflammation, dilate and move the pupil to avoid posterior synechiae formation, and eliminate the inciting cause. Medical therapy is usually similar to that for acute uveitis, but can include the addition of immunodulators or immunosuppressives, such as cyclosporine or azathioprine, for certain cases. Other therapy includes target therapy for the underlying etiology if it has been determined. Paired with often characteristic systemic clinical signs, anterior uveitis is part of many systemic diseases, and these ocular signs are very helpful in establishing the clinical diagnosis. Laboratory tests can help to confirm the specific disease. Rocky Mountain spotted fever (RMSF) is caused by Rickettsia rickettsii and carried by ticks, Dermacentor andersoni, D. variabilis, and Amblyomma americanum. It produces a vasculitis and platelet deficiency that is shown clinically as diffuse hemorrhages that affect many organs. Hemorrhages and inflammation can affect the conjunctiva, anterior and posterior uvea, retina, and optic nerve head (Figure 10.8; see also Figure 3.15E). The uveitis usually develops 2–3 weeks postinfection. Serology tests, especially when paired, are useful in making the diagnosis. There are several other tick‐borne infections that can cause uveitis, including ehrlichiosis, anaplasmosis, and borreliosis. Figure 10.8 Anterior uveitis with hemorrhage of the iridal surface in a dog infected with Rickettsia rickettsii. The immature (fourth stage) larvae of Dirofilaria immitis is the most frequent intraocular parasite in the dog in North America (Figure 10.9
Canine Anterior Uvea
Congential Variations and Disorders
Heterochromia Iridis
Persistent Pupillary Membranes
Iridal Nests or Iridal Arrests
Iridal Hypoplasia and Colobomas
Inflammations of the Anterior Uvea
Acute Uveitis
Chronic Uveitis
Specific Types of Anterior Uveitis
Anterior Uveitis and Rocky Mountain Spotted Fever
Anterior Uveitis and Heartworm (Dirofilaria immitis)
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