Download 2. Infectious uveitis

I.
Immune Response
1. Class I, Class II
2. HLA Associations
3. Immune Processing: Lymph Nodes
4. Cytotoxic & Delayed Hypersensitivity
5. Hypersensitivity Reactions; Types 1-5
II. Ocular immune Response
1. Conjunctiva
2. Cornea
3. Anterior Chamber
4. Lens: phacogenic uveitis
5. Uveal Tract: four types immune reactions
6. Retinal Antigens and Auto-immune Uveitis
A. Modulation of Immune Response
Homeostatic mechanisms:negative feedback
B. Medications: immune therapies
Inflammatory Cascade: Arachadonic acid pathway, cyclooxygenase pathway
III. Ocular Complications: Visual Loss
1. Cataract
2. Glaucoma
3. Uveitic: open or closed angle
4. Neovascular
5. CME, ERM, atrophy
6.
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9.
Serous RD
CNVM
Vaso-occlusive disease
Optic Nerve Edema or atrophy
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Bilateral > 50%
Recurrences common
Typically affects anterior segment
blood supply
IV. Clinical cases:
Case 1: The Red Eye
Differential ?, Diagnosis ?, Management ?, Labs ?
A. Discussion: Scleritis
1. Severe, rapid, destructive disease
2. Most common in fourth to sixth
decades of life
3. F > M
a) Types:
1. Diffuse Anterior Scleritis: most common and relatively benign
2. Nodular Anterior Scleritis: immovable scleral tissue, very tender
3. Necrotizing Anterior Scleritis with Inflammation: extreme pain, high risk
4. sclera progressively thins
5. Necrotizing Anterior Scleritis w/out Inflammation: effects of inflammation w/out
symptoms
6. Posterior Scleritis: orbital disease
b) Clinical Evaluation:
1. Sectoral or diffuse injection at all levels of vessels
2. Blue hue in natural light
3. Vessels do not blanche/move
c) Scleritis Management
1. Internal medicine/rheumatology consult
2. Etiology:
3. Lab testing: 50% systemic disease identified
4. Management: Drugs
B. Discussion: Episcleritis
1. Benign, transient, & self-limited
2. Young adults 20 to 50Mean 43
3. Female > male 7:3
4. 1/3 bilateral
5. 70% idiopathic
6. Fiery red or brick red to mild flush
injection
7. Conjunctival vessels blanche and
movable
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11.
16% nodular form
28% recurrent
Associated systemic disease was found in 1/3 of the patients (36%)
One-half of patients have concurrent other ocular involvement, including uveitis
(13%), glaucoma (5%), and keratitis (13%)
a) Clinical Evaluation:
1. Sectoral injection 70%
2. Diffuse injection 30%
b) Types:
1. Simple episcleritis: 80%
2. Nodular episcleritis: localized,variable tenderness
c) Management:Lab testing generally not performed
Topical therapy, Oral therapy
Case 2: The Redder Eye
Differential ?, Diagnosis ?, Management ?, Labs ?, missing history?
a) Uveitis Location
1. Anterior: iritis vs iridocyclitis
2. Intermediate: pars planitis
3. Posterior
4. Panuveitis
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
Acute:Release of vasoactive substances
Chronic:Non-granulomatous vs granulomatous
b) Symptoms
c) Clinical Signs

inflamed eye

circumlimbal flush

cell & flare
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KP- Arlt’s sign

IOP change
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Synechia
heterochromia
iris nodules
miosis
neovascularization
iris atrophy
retinal & ONH changes
A. Discussion: Etiology:Non-granulomatous vs Granulomatous
B. HLA-B27
1. Anklyosing Spondylitis (>90%)
2. Reiter’s Syndrome (75%)
3. Inflammatory Bowel Disease (50-75%)
4. Psoriatic Arthritis (10-70%)
a)HLA-B27 Related Diseases
1. Second commonest cause of anterior uveitis
2. 40 to 70% of cases of acute anterior uveitis
3. Inflammation may be more severe than that found in idiopathic anterior uveitis
4. Fibrinous reaction (25%)
5. Hypopyon (14%)
6. Formation of posterior synechiae
Case 3.The new patient walks in and sits in your chair
1. Diagnosis ?, Management ?, Labs ?
2. Infectious uveitis
3. Etiology / epidemiology- Ocular Syphilis
Case 4. Inflammation and a cough
1. Diagnosis ?, Management ?, Labs ?
2. Etiology / epidemiology: Ocular tuberculosis
Case 5. The case of the chronic inflammation
1. Diagnosis ?, Management ?, Labs ?
Discussion: Ocular sarcoidosis
A. Etiology:
1. Granulomatous inflammation of unknown cause
2. Multisystem involvement: can affect any organ in the body, preferently lungs, thoracic
lymph nodes, skin and eyes
3. Ocular involvement may precede extraocular manifestations by as many as 8 yrs.
4. 25-50% of patients will eventually have an ocular manifestation
Ocular
1.
2.
3.
4.
Sarcoidosis
Age:20-60
F>M
Genetic influence: HLA-B8?/Environmental factors
Mortality: 0.5-5%
a) Systemic manifestations:
1. Respiratory 80-90%
2. Lymph nodes: 76%
3. Skin 22%
4. Liver/ spleen: 20%
5. CNS: 8%
6. Arthralgias/ arthritis: 37%
b) Ocular manifestations:
1. 25-75%
2. 2-5% of all uveitis
c) Anterior segment (85%):
1. Conjunctival nodules 7%
2. Iris nodules: 35%
3. Iritis 52%
4. Cyclitis and nodules in ciliary body:
42%
d) Posterior segment (30%)
1. Vitritis, “snoballs”: frequent
2. Retinal phlebitis: 20%
3. Macular edema: frequent
4. Neovascularization
5. Granulomas in the angle: 50%
6. Glaucoma: 23%
7. Cataract: 17%
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8.
Choroidal/retinal granuloma
Retinitis: rare/chorioretinitis:11%
Arteriolitis: rare
Disc edema/papillitis:7%
Fuch’s heterochromic iridocyclitis
Herpetic disease
Last case to test your knowledge..
V. Laboratory testing: Used if:
1. Recurrent
2. Bilateral
3. chronic
4. medically unresponsive
5. condition becomes granulomatous
6. deeper forms of uveitis
7. Signs / Sx underlying systemic Dz
VI. Uveitis Treatment
A. purpose:
1. Reduce the severity of the inflammation;
2. Prevent posterior synechiae and permanent structural change to the iris blood vessels
and blood-aqueous barrier;
3. Reduce the frequency of attacks if the disease is chronic;
4. Protect the macula, optic nerve, and vitreous; and
5. Prevent the loss of ciliary body or retinal function.
B. Goal:
1. Complete elimination of all active inflammation
2. Chronic inflammation eventually produces structural damage to ocular tissues
3. Limitation of total steroid needed
4. Long term treatment has a 100% incidence of side effects
C. General treatment principles
1. Urgent care: steroids, cycloplegics, antihypertensives
2. Stress management
3. Dietary and other lifestyle alterations- adequate rest and exercise
4. Define goals both short and long term with patient
5. Risk / benefit ratios
6. Step-ladder approach: steroids, NSAIDS, immunosuppressants
7. Therapy for macular edema
D. Medical Therapy
1. Use enough medication, soon enough to get total suppression of inflammation with
eventual tapering and discontinuation
2. Use topical and systemic NSAIDS as steroid-sparing agents.
a) Step ladder approach:
1. Steroids first
2. NSAIDS added if pt. relapses with attempted steroid withdrawal
3. Systemic immunosuppresive therapy in steroid resistant or if unacceptable
side effects occur
4. Selected diseases
b) Goals:
1. Reduce inflammation
2. Patient comfort
3. Lessening of complications
4. Preserve or improve vision
c. Treatment types:
1. Topical- drops or ointment
2. Regional- periocular injection
3. Systemic- po or IV
4. Intraocular- injection/implant
5. Immunosupressive chemotherapy
steroid