NAVLE Special Senses

Canine Uveitis Study Guide

📅 March 28, 2026 ⏱ 25 min read

Overview and Clinical Importance

Uveitis refers to inflammation of the uveal tract, which comprises the iris, ciliary body, and choroid. It is one of the most common and clinically significant ocular diseases encountered in canine practice. The uvea is the highly vascular middle layer of the eye responsible for producing aqueous humor, regulating pupil size, and providing nutrients to the retina.

Uveitis can be classified anatomically as anterior uveitis (inflammation of the iris and ciliary body, also called iridocyclitis), posterior uveitis (inflammation of the choroid, also called choroiditis), or panuveitis (inflammation involving all three structures). Anterior uveitis is the most commonly diagnosed form in dogs.

High-YieldApproximately 40-60% of canine uveitis cases are idiopathic or immune-mediated in origin. Always consider systemic disease when bilateral uveitis is present.

Category	Examples	Key Features
Immune-Mediated/Idiopathic	Idiopathic uveitis, uveodermatologic syndrome (VKH-like), lens-induced uveitis, Golden Retriever pigmentary uveitis	Most common category (approximately 75% of cases). Diagnosis of exclusion. May require lifelong treatment.
Infectious - Tick-borne	Ehrlichiosis (E. canis), Rocky Mountain spotted fever, Lyme disease (Borrelia)	Often bilateral. Associated with thrombocytopenia, hyphema. Test in endemic areas.
Infectious - Fungal	Blastomycosis, histoplasmosis, cryptococcosis, coccidioidomycosis	Geographic distribution. Often involves posterior segment (chorioretinitis). Look for respiratory signs.
Infectious - Bacterial	Leptospirosis, brucellosis, septicemia, pyometra-associated	Leptospirosis: hepatic and renal signs. Brucellosis: reproductive signs. Primary bacterial uveitis is rare.
Neoplastic	Lymphoma (most common metastatic), uveal melanoma, iridociliary adenoma/adenocarcinoma	Lymphoma: check peripheral lymph nodes. May see iris thickening, hyphema, dyscoria. Aqueous cytology can be diagnostic.
Traumatic/Reflex	Blunt or penetrating trauma, corneal ulceration (reflex uveitis), foreign body	Usually unilateral. Corneal ulcer causes mild reflex uveitis via axonal reflex and prostaglandin release.
Lens-Induced	Phacolytic (cataract protein leakage), phacoclastic (lens capsule rupture)	Common in diabetic cataracts. Phacoclastic more severe. Treat uveitis before cataract surgery.

Pathophysiology

Blood-Aqueous Barrier (BAB)

The blood-aqueous barrier (BAB) is maintained by tight junctions between the non-pigmented ciliary epithelium and the posterior iris epithelium, as well as the endothelium of iris blood vessels. This barrier normally prevents proteins and cells from entering the aqueous humor.

When the uveal tract becomes inflamed, the BAB breaks down, allowing proteins, fibrin, and inflammatory cells to leak into the aqueous humor. This is visualized clinically as aqueous flare (the Tyndall effect) when a focused beam of light is directed into the anterior chamber.

NAVLE TipThe presence of aqueous flare is PATHOGNOMONIC for uveitis. If you see aqueous flare on exam, you have confirmed uveitis - now determine the cause!

Inflammatory Cascade

Uveitis triggers the release of prostaglandins (especially PGE2) and other inflammatory mediators. Prostaglandins cause vasodilation of deep episcleral vessels (ciliary flush), breakdown of the BAB, miosis via pupillary sphincter stimulation, and decreased aqueous humor production leading to ocular hypotony.

The inflammatory process occurs in three phases: acute/active phase (exudative, with serous, fibrous, bloody, or purulent exudate), subacute phase (immune reaction begins), and chronic phase (may result in scarring, necrosis, recurrence, or chronicity).

Sign	Description	Clinical Significance
Aqueous Flare	Tyndall effect - light beam visible traversing anterior chamber (like headlights in fog)	PATHOGNOMONIC for uveitis. Indicates BAB breakdown. Best seen with slit lamp in darkened room.
Miosis	Constricted pupil due to ciliary muscle spasm and prostaglandin release	Important differentiator from glaucoma (mydriasis). Causes significant pain.
Low IOP (Hypotony)	Typically less than 10-15 mmHg due to decreased aqueous production from ciliary body inflammation	CRITICAL differentiator from glaucoma. Normal or elevated IOP in inflamed eye suggests secondary glaucoma.
Ciliary Flush	Deep perilimbal episcleral vessel engorgement (radially oriented vessels around limbus)	Does not move with conjunctiva. Does not blanch with topical epinephrine (unlike conjunctival vessels).
Rubeosis Iridis	Neovascularization and hyperemia of iris surface giving reddish appearance	Indicates chronic uveitis. Fragile new vessels may cause hyphema.
Hyphema	Blood in anterior chamber - may settle ventrally or fill chamber	Consider trauma, coagulopathy, neoplasia, ehrlichiosis. Avoid NSAIDs if present.
Hypopyon	White blood cells/pus settling in ventral anterior chamber	Indicates severe inflammation. Consider infectious cause or severe immune response.
Keratic Precipitates	Inflammatory cell aggregates on corneal endothelium (usually ventral one-third)	"Mutton fat" precipitates suggest granulomatous inflammation (FIP in cats, blastomycosis).
Corneal Edema	Cloudiness due to endothelial dysfunction from inflammation	May be focal (at keratic precipitates) or diffuse. May obscure visualization of deeper structures.

Etiology and Classification

Uveitis causes are classified as exogenous (external causes such as trauma or corneal ulceration) or endogenous (internal causes including infections, neoplasia, and immune-mediated disease).

Major Categories of Canine Uveitis

Exam Focus: For NAVLE, remember that BILATERAL uveitis strongly suggests systemic disease (infectious or immune-mediated), while UNILATERAL uveitis is more likely traumatic or lens-induced.

Suspected Cause	Recommended Tests
Fungal disease	Blastomyces, Histoplasma, Coccidioides serology or urine antigen; thoracic radiographs
Leptospirosis	MAT titers (paired, 2-4 weeks apart), PCR on blood or urine
Brucellosis	RSAT, culture (blood, reproductive tissues); consider in intact dogs with reproductive signs
Neoplasia	Lymph node aspirate, abdominal ultrasound, aqueous centesis cytology
Toxoplasmosis	Toxoplasma gondii serology (IgM and IgG)
UDS confirmation	Skin biopsy from depigmented area (lichenoid interface dermatitis with pigmentary incontinence)

Clinical Signs and Examination Findings

Clinical signs of uveitis can be categorized into signs of ocular discomfort, signs specific to anterior uveitis, and signs of posterior uveitis.

Signs of Ocular Discomfort (Non-specific)

Blepharospasm - squinting due to pain
Photophobia - light sensitivity
Epiphora - excessive lacrimation
Enophthalmos - globe retraction from pain

Anterior Uveitis - Cardinal Signs

High-YieldThe classic triad of anterior uveitis is: (1) Aqueous flare, (2) Miosis, and (3) Low IOP. This triad distinguishes uveitis from glaucoma, which presents with mydriasis and elevated IOP.

P - Photophobia

A - Aqueous flare (pathognomonic)

I - IOP decreased (low pressure)

N - Narrowed pupil (miosis)

F - Flush (ciliary)

U - Uveal swelling/redness (rubeosis)

L - Lacrimation and blepharospasm

Drug Class	Examples	Dosing	Key Notes
Corticosteroids	Prednisolone acetate 1%, Dexamethasone 0.1%	q4-6h initially, taper as inflammation resolves	FIRST-LINE. CONTRAINDICATED with corneal ulcer. Best corneal penetration.
NSAIDs	Diclofenac 0.1%, Flurbiprofen 0.03%, Ketorolac 0.5%	q6-12h	Use with steroids in severe cases, or alone if steroids contraindicated. Avoid with hyphema.
Mydriatics/Cycloplegics	Atropine 1%, Tropicamide 1%	Atropine: q6-24h to effect; Tropicamide: q6-12h	Prevents synechiae, relieves ciliary spasm pain, stabilizes BAB. Monitor IOP - discontinue if glaucoma develops.

Breed-Specific Uveitis Syndromes

Golden Retriever Pigmentary Uveitis (GRPU)

Golden Retriever Pigmentary Uveitis (GRPU) is a unique, inherited ocular condition affecting Golden Retrievers. It is suspected to be autosomal dominant with incomplete penetrance. The prevalence of uveal cysts is approximately 34% and pigmentary uveitis affects approximately 5.5-18% of older Golden Retrievers.

Key Clinical Features:

Radial pigment deposition on the anterior lens capsule (DEFINITIVE diagnostic criterion)
Thin-walled uveal cysts (iris and ciliary body) - present in 13-42% of affected eyes
Chronic, low-grade inflammation
Mean age of onset: 8.5 years (late-onset disease)
Usually bilateral
High risk of secondary glaucoma (21-45%) and vision loss (approximately 50% within one year)

NAVLE TipFor Golden Retrievers with uveitis, look for radial pigment on the anterior lens capsule - this is the hallmark finding. Uveal cysts alone do NOT confirm GRPU. Annual ophthalmologist exams are recommended for all breeding Golden Retrievers.

Uveodermatologic Syndrome (VKH-like Syndrome)

Uveodermatologic Syndrome (UDS) is an immune-mediated disease targeting melanocytes in the uveal tract, skin, and hair follicles. It is analogous to Vogt-Koyanagi-Harada syndrome in humans but typically lacks neurologic involvement in dogs.

Breed Predisposition: Akitas (66-80% of cases), Siberian Huskies, Alaskan Malamutes, Samoyeds, Chow Chows, and other Nordic breeds. Also reported in Shetland Sheepdogs, Australian Shepherds, Irish Setters, Bernese Mountain Dogs, and others.

Key Clinical Features:

Ocular signs (usually first): Severe bilateral panuveitis, blepharospasm, photophobia, conjunctival hyperemia, aqueous flare
Dermatologic signs: Leukoderma (depigmentation) of nose, lips, eyelids, footpads, scrotum; leukotrichia (whitening of hair/poliosis)
Median age of onset: 4.1 years (young to middle-aged)
Male predisposition (approximately 66%)
High risk of blindness without aggressive treatment

Treatment: Aggressive systemic immunosuppression (prednisone 1-2 mg/kg daily, often combined with azathioprine 2 mg/kg daily) plus topical corticosteroids and mydriatics. Treatment is typically lifelong. Prognosis for vision is guarded to poor.

A - Akita (and Arctic/Nordic breeds)

K - Keratoprecipitates and KCS possible

I - Immune-mediated (attack on melanocytes)

T - Two systems (eyes AND skin)

A - Aggressive immunosuppression needed for life

Drug Class	Examples	Dosing	Indications
Corticosteroids	Prednisone/Prednisolone	Anti-inflammatory: 0.5-1 mg/kg/day; Immunosuppressive: 1-2 mg/kg/day	Posterior uveitis, immune-mediated disease, severe anterior uveitis. Rule out infection first.
NSAIDs	Carprofen, Meloxicam	Standard labeled doses	Mild uveitis, suspected infection. NEVER combine with systemic steroids (GI ulceration risk).
Immunosuppressives	Azathioprine, Cyclosporine, Mycophenolate	Azathioprine: 2 mg/kg/day initially	Steroid-unresponsive immune-mediated uveitis (UDS). Monitor CBC for myelosuppression.
Antimicrobials	Doxycycline, Itraconazole, Fluconazole	Doxycycline: 5-10 mg/kg q12-24h; Antifungals: varies	Doxycycline for tick-borne disease. Antifungals for systemic mycoses (often months of treatment).

Diagnostic Approach

A systematic diagnostic approach is essential because uveitis is often a manifestation of systemic disease. The diagnostic workup should be tailored based on whether uveitis is unilateral versus bilateral, and whether the patient has concurrent systemic signs.

Complete Ophthalmic Examination

Menace response and visual assessment: May be diminished with severe inflammation
Pupillary light reflexes: Sluggish or absent due to posterior synechia or iris swelling
Schirmer tear test: Atropine use decreases tear production
Tonometry: ESSENTIAL - expect low IOP (less than 10-15 mmHg); normal or elevated IOP suggests secondary glaucoma
Fluorescein stain: ALWAYS perform to rule out corneal ulceration (contraindicates topical steroids)
Slit lamp examination: Best for detecting aqueous flare, keratic precipitates, anterior lens pathology
Indirect ophthalmoscopy: Funduscopic exam after dilation (if IOP acceptable) to assess posterior segment
Ocular ultrasound: If posterior segment cannot be visualized; assess for retinal detachment, masses, lens pathology

Minimum Database for Uveitis

The following tests are recommended for ALL patients with uveitis:

Complete blood count (CBC): Thrombocytopenia (ehrlichiosis, IMTP), leukocytosis/leukopenia
Serum chemistry profile: Azotemia (leptospirosis), hyperglobulinemia (ehrlichiosis, multiple myeloma)
Urinalysis: Proteinuria, isosthenuria
Tick-borne disease panel: SNAP 4Dx or equivalent (Ehrlichia, Anaplasma, Lyme, Heartworm)
Thoracic radiographs: Pulmonary fungal patterns, metastatic disease, lymphadenopathy

Additional Testing Based on Clinical Suspicion

Exam Focus: Aqueous centesis (aqueocentesis) can be performed by an ophthalmologist for cytology (lymphoma, neoplasia) or culture. The Goldman-Witmer coefficient compares aqueous:serum antibody titers - a ratio greater than 1 indicates intraocular antibody production confirming ocular infection.

Complication	Mechanism	Clinical Impact
Posterior Synechia	Adhesions between iris and anterior lens capsule due to inflammation and miosis	Can cause irregular pupil (dyscoria). Complete 360-degree synechia causes iris bombe and secondary glaucoma.
Secondary Glaucoma	Inflammatory debris clogs drainage angle; peripheral anterior synechia; pupillary block from iris bombe	MOST IMPORTANT complication. Can occur acutely or chronically. Irreversible vision loss if not treated promptly.
Cataract Formation	Inflammatory damage to lens metabolism; zonular disruption	Common with chronic uveitis. Creates a cycle: cataracts cause lens-induced uveitis.
Lens Luxation	Inflammatory degradation of lens zonules	Anterior luxation is an emergency (causes acute glaucoma). Posterior luxation less urgent.
Retinal Detachment	Subretinal exudate accumulation from chorioretinitis; traction from vitreal bands	Causes blindness. May be exudative (inflammatory) or tractional.
Phthisis Bulbi	End-stage shrunken, non-functional globe from chronic inflammation	Irreversible. Enucleation often recommended for comfort.

Treatment

Primary treatment goals: (1) Halt inflammation, (2) Stabilize the blood-aqueous barrier, (3) Minimize sequelae, (4) Decrease pain, and (5) Preserve vision. Treatment should begin immediately at diagnosis, even before completing the diagnostic workup.

Topical Therapy

Systemic Therapy

High-YieldTreatment should continue for 2-4 WEEKS BEYOND resolution of clinical signs. Premature discontinuation leads to recurrence. Always taper gradually rather than stopping abruptly.

Complications and Sequelae

Uncontrolled or chronic uveitis can lead to several vision-threatening complications. Client education on these potential sequelae is essential to ensure compliance with treatment and follow-up.

NAVLE TipIf you measure NORMAL or ELEVATED IOP in an eye with active uveitis, suspect SECONDARY GLAUCOMA. This is a critical finding because it indicates the inflammation has compromised aqueous outflow.

Prognosis

Prognosis depends heavily on the underlying cause, severity of inflammation, duration before treatment, and development of complications. With proper treatment, most cases of uveitis begin to improve within 24-48 hours.

Acute, single-episode, treated promptly: Good prognosis for vision retention
Infectious causes: Guarded to good with appropriate antimicrobial therapy
Chronic/recurrent uveitis: Guarded due to cumulative damage and complication risk
GRPU: Guarded - approximately 50% vision loss within 1 year of diagnosis
UDS: Guarded to poor - blindness common even with aggressive treatment
Secondary glaucoma: Poor once developed - often leads to enucleation

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