SECTION 2: THE UVEA

ANATOMY
Consists of: iris anteriorly; ciliary body and choroid posteriorly; in continuity with each
other
Definition: Pigmented highly vascular layer lying between retina and sclera
Concerned with:
1. Nutrition of eye ciliary body epithelium secretes aqueous humour
2. Maintenance of outer retina from choroidal circulation
Uveitis: inflammation of uvea; damage may occur to vascular epithelium in this tissue >
breakdown of blood-aqueous barrier
CLASSIFICATION
Iritis
inflammation of iris; anterior uveitis
Cyclitis
Inflammation of ciliary body; intermediate uveitis
Choroiditis Inflammation of choroid; posterior uveitis
Iridocyclitis
Inflammation of iris and ciliary body
Retinochoroiditis/chorioretinitis
Inflammation involving retina and choroid
-

Classification according to:

a. Anatomy
b. Histopathology (3rd year path)

Anterior uveitis
Most symptomatic
Pain
Photophobia
Red eye
Observe cells and flare
Non-granulomatous allergic type
reaction
More acute; sudden onset
No posterior involvement
Small keratic precipitates
EG: Ankylosing spondylitis

Posterior uveitis
Less symptomatic
Less pain

Cells in vitreous
Granulomatous

Insidious onset
Retina and choroid involved
Larger keratic precipitates
EG: Sarcoidosis, toxoplasmosis

*Uveitis question
Differentiate between iridocyclitis and chorioretinitis (6)
Signs and symptoms most likely associated with iridocyclitis or chorioretinits: red eye,
insidious onset, cells and flare, pain, small KPs, large KPs, vitreous haemorrhage,
photophobia

CONGENITAL ABNORMALITIES OF UVEA

1. Iris Coloboma:
Incomplete structural formation
Defects off closure of optic cup
7-8 weeks foetal
Can be sectorial from trivial to gross
Usually inferio-nasally
May involve iris, choroid, retina or optic disc
2. Aniridia:
Can be genetic (autosomal dominant)
Associated with:
a. Glaucoma (due to perirpheral anterior synechiae)
b. Nystagmus
c. Corneal opacities
d. Photophobia
3. Polycoria
More than one pupil
Most often acquired (trauma or surgically pseudopolycoria)
4. Ectropion uvea
Produced by endothelial traction and peripheral anterior synechiae
Due to primary disorder of corneal endothelium
5. Corectopia:
Displaced/eccentric pupil
Associated with primary disorder of corneal endothelium
6. Anisocoria:
Both pupils not same size
Types:
a. Essential anisocoria: 20% show small differences in pupil size
b. Pathological:
Caused by lesions affecting sympathetic or parasympathetic pathways or
by local iris disease
Refer pupil reactions
Aetiologies: 1. Horners; 2. Adies; 3. Trauma; 4. Oculomotor palsy; 5. Local
inflammation or infection
Management: rule out Adies and Horners
1. Determine duration (evaluate old photos)
2. Follow up within 72h
3. Complete threshold visual fields
4. Stereoscopic optic nerve head evaluation
5. Check for Mothers atropine syndrome

ANATOMY OF PUPILLARY LIGHT REFLEX

1. Iris dilator muscle:
Bordering pigment epithelial layer of iris back surface, posterior layer
Responds to sympathetic stimulation (through CNS) pupil dilates
2. Iris sphincter muscle:
Not as affected by pigment binding drugs
Arranged in 1mm circular band at pupillary margin
Responds to PSM stimulation
Accommodation, light reflex and orbicularis action
3. Parasympathetic pathway: (pupil constriction)
Stimulated by light imaged on retina or accommodation
Afferent fibres travel in optic nerve > cross chiasm like visual fibres > synapse in
pretectal nucleus
Second order neuron synapses in vicinity of Edinger Westphal Nucleus (part of
dorsal aspect of oculomotor nucleus)
Third order neuron synapses in ciliary ganglion and final neuron innervates iris
sphincter muscle (terminates there) > controls pupil and ptosis
4. Sympathetic pathway: (pupil dilation)
Stimulated by fright, flight, d darkness and other emotions
Starts in hypothalamus > sympathetic first order neuron travels in cervical area >
synapses in ciliospinal centre of Budge (C8 T2)
Second order neuron travels over apex of lung > synpases in superior cervical
ganglion (neck)
Third order neuron parallels internal carotid artery > joins ophthalmic division of
trigeminal nerve > innervates dilator muscle via nasociliary and long ciliary nerves

PUPIL ABNORMALITIES
Causes of bilateral LND
1. Neurosyphilis
2. Type 1 diabetes
3. Parinauds syndrome
4. Myonic dystrophy
5. Familial amyloidosis
6. Encephalitis
7. Chronic alcoholism

Causes of unilateral LND

1. Adies Pupil
2. Herpes Zoster
3. Afferent conduction defect
4. Aberrant regeneration of CNS

1. Essential anisocoria: refer anisocoria notes

2. Amaurotic Pupil:
Occurs in eye with no light perception (i.e. blind)
Due to ocular or ON disease (any ON lesion)
Signs:
Both pupils equal size
Neither pupil reacts to light stimulus in affected eye (no direct reflex)
Both pupils react to light stimulus in normal eye (consensual reflex)
Near reflex normal in both eyes
*Amaurotic Pupil question
Pupil reactions in twenty year old: (3)
Reaction to near stimulus = normal
Pupil size = 5mm OU
Light stimulus in RE = 5mm OU
Light stimulus in LE = 3mm OU
-

a. State tentative diagnosis for pupil conditions

Amaurotic pupil
b. Most probable aetiology
ON disease/lesion
c. VA expected in each eye
No light perception

3. Midbrain tectal pupil

Due to compressive lesions of third ventricle
Pupils moderately larger than normal; may be eccentric
Usually associated with Parinauds dorsal midbrain syndrome > impairment of
upward gaze caused by damage to vertical gaze centre
Usually has LND and convergence-retraction nystagmus

4. Marcus Gunn Pupil: (afferent)

Relative afferent defect/ afferent pupillary defect
Clinical:
Detected using swinging flashlight test; confirm with red desaturation test
In absence of gross ocular disease, implies incomplete neurological lesion in
anterior visual pathway
Due to less stimulation to EW nucleus
Results from loss of sensitivity or large numbers of axons in optic nerve
RAPD not produced when both optic nerves are equally damaged or with
opacities in ocular media (cataract)
Signs:
Perception > light intensity of source less > affected pupil dilates accordingly >
reflects degree of impairment
Vision may not be proportionally reduced
Aetiology:
Can be observed with dense vitreous haemorrhages and dense amblyopia
Optic neuritis
AION
Very asymmetrical glaucoma
Maculopathies
Permanent optic neuropathy with loss of significant portion of papillary macula
bundle
Swinging flashlight test:
Each pupil stimulated in rapid succession
When abnormal pupil is stimulated, it dilates instead of constricting
Withdrawal of light from normal eye (consensual dilation) outweighs stimulation
to abnormal eye(constriction) > paradoxical reaction of pupil to light
5. Argyll-Robertson Pupil:
Aet: Syphilis (hallmark of neuro-syph)
Signs:
Both pupils affected
LND
Pupils nearly always small and irregular
Dilate poorly after mydriatic instillation (lesion between pre-tectal nucleus
and EW nucleus)
DDX: (for LND)
a. Tabes diabetic
b. Tabes pituitaria
c. Adies pupil

6. Fixed dilated pupil (internal ophthalmoplegia)

Probably secondary to ciliary nucleus damage
Aetiology:
a. Varicella botulism
b. Post pan retinal photo-coagulation
c. Compression/aneurism off posterior communicating artery
Third nerve palsy: MR, IO, SR, IR, Levator muscle
1. Pupillary sparing (always vascular)
Pupil spared because pupillary fibres are close to blood supply and within
ONH
Signs: Diplopia (down and out) with huge ptosis and normal pupil size and
reflexes
Aet: Diabetic oculomotor or vascular disease oculomotor palsy
Tx: Consider treatment for underlying cause, but condition will
spontaneously resolve in 6 weeks
2. Non-pupil sparing (internal ophthalmoplegia; fixed, dilated)
Signs: Total palsy and complete ptosis
Tx: Consider occupying lesion and immediately refer to neurologist to
prevent rupture of possible aneurism
Aet: Compression of aneurism on posterior communicating artery
*Fixed Dilated Pupil Questions
Painful third nerve palsy and fixed dilated pupil (11)
a. Possible aetiologies
b. If presented with pupil sparing > most likely associated systemic conditions
c. Which condition requires urgent referral? Motivate
Non-pupil sparing
7. Horners syndrome (Efferent pupil defect oculosympathetic palsy)
Aet:
a. Apical lung tumour (Pancoast tumour)
b. Chest trauma, neck surgery
c. Congenital/early infancy (presents here with heterochromia)
d. Other intra-cranial lesions
Signs
Unilateral triad: ptosis, miosis and anhydrosis (if below superior cervical
gang)
More marked in dim illumination
Apparent enophthalmosis (on affected side) > due to ptosis (upper) and
elevation of lower lid (paralysis off smooth muscle in tarsal plate)
Increased amplitude of accommodation due to unopposed PSM innervation
Test:
a. 1 drop cocaine 4% to each eye
b. Affected eye will not dilate but normal eye will
c. If Horners is found > two days later, test is done to locate where lesion is
d. 1 drop Hydroxyamphetamine 1%/ Paradrine 1% to each eye wait 20m
e. In pre-ganglionic lesion > affected pupil dilates twice as much as normal eye >
chest x-ray for lung tumour
f. Post ganglionic lesion > affected pupil doesnt dilate
8. Adies Pupil (Tonic pupil)
Prevalence: Females 30-50
Presentation: Unilateral 80%, benign, common

 Sx:
a. Dilated pupil
b. decreased accommodation (proximal blurred vision)
c. minimal light reflex
signs:
a. classic vermiform reaction of iris sphincter under slit lamp
b. Slow and tonic redilation (residual miosis)
c. May have LND
d. Deep tendon reflex absent/reduced
Aet:
Recent cold/viral infection, especially upper respiratory tract
Denervation of post-ganglionic nerve supply to sphincter > lesion in ciliary
ganglion (knocks out PSM)
Diagnosis:
Instill 1 drop of 1.125% pilocarpine in each eye (stimulates PSM innervation)
Affected pupil will contract in 30m due to denervation sensitivity
Normal pupil wont react
*Adies Pupil Question
Twenty two year old woman > decreased vision at near + okay distance vision + mild cold +
slight cough + unequal pupil size(10)
a. Most likely conditions and other possible clinical findings
b. Ophthalmic preparation used to confirm diagnosis. Explain

*Adies pupil and Horners Question

Adies pupil and Horners Syndrome = acquired pupil anomalies (4)
- Which nervous system is affected in each?
Adies = PNS
Horners = SNS
- What tests are utilized in each?
Adies = 1.125% pilocarpine
Horners = 4% cocaine or 1% Hydroxyampetamine/Paradrine

IRIS PIGMENT ABNORMALITIES

1. Brushfields spots:
Light coloured condensations of surface of mid-iris; Downs
2. Heterochromia iridis (see third year path)
Waardenburg-klein syndrome
Albinism-deafness syndrome
Associated with hypopigmentation and alopecia
Also seen in Turks retraction syndrome
Congenital Horners
Heterochromic iridocyclitis of Fuchs (see third year path)
Forms minority of anterior uveitis (2%)
Hypo/hyper-chromic
70% unilateral; no posterior synechiae form
Sx:
a. Fine widespread kps over whole of corneal endothelium (looks fluffy)
b. Iris = moth eaten appearance
c. Px is asymptomatic until iris atrophies (pupil may be larger)
d. Vision decreases due to cataract formation
e. Secondary glaucoma occurs due to sclerosed trabecular meshwork
Aetiology unknown
3. Albinism:
Due to deficiency of melanin within uveal tract
Occurs in following forms:
a. Ocular albinism:
X-linked
Rarely recessive
Very translucent irises
Cutaneous (skin and hair) pigmentation is normal
b. Oculocuatenous albinism:
Tyrosine negative: Complete absence of pigment
Tyrosine positive: more normal skin and ocular pigment, often with light
brown/reddish hair; paler than other family members
c. Cutaneous albinoids:
If purely cutaneous, no ocular problems
Ocular involvement:
a. Increased iris transillumination
b. Hypopigmented fundi
c. Congenital nystagmus
d. Macular hypoplasia
e. High incidence of squint and amblyopia
f. Chiasmic anomaly where majority of fibres decussate

ACQUIRED ABNORMALITIES
- First two conditions: observed with iris transillumination due to fundus reflex shining
through iris
- All can be observed with gonioscopy in viewing the angle
1. Pseudoexfoliation syndrome:
Presentation: 20%; Usually unilateral; more common in females
Signs:
Grey/white precipitates on and within anterior lens capsule
Characterized by appearance of central circular area of normal lens capsule,
surrounded by clear ring, surrounded by circular grey area > seen clearly
once pupil is dilated > Bulls eye appearance
Flaky dandruff material is histochemically of amyloid material
Tip of iris rubs on amyloid and pigment is released into aqueous > deposited
into TM > TM becomes more pigmented, but no amyloid seen in TM
Amyloid can be deposited onto corneal endothelium > more inferiorly due to
convection currents > Krukenberg spindles
Zonules weakened > on dilation, IOP goes up
Aet:
Thought to be related to aging abnormality of generalized basement
epithelial membrane cells
More commonly seen in fair/Scandinavian patients
Complication:
20% develop pigmentary glaucoma
2. Pigment Dispersion syndrome:
Aet: Occurs more frequently in young myopic males
Clinical:
Zonular rubbing > shedding of iris pigment into aqueous > TM
Iris transillumination and Krukenbergs spindles
Pigment seen as darkly pigmented band in filtration portion of TM > confined
to relatively smooth bordered circumscribed band
20% develop pigmentary glaucoma

*PEX and PDS question

Similarities and differences between pigment dispersion syndrome and pseudoexfoliation
including expected gonioscopy findings (6)
PEX
PDS
20% of patients develop PEX
20% of patients develop pigmentary
glaucoma
Usually unilateral, more common in
Occurs more frequently in young myopic
females and fair px
males
Lens:
No lens observations
1. Bulls eye appearance
2. Grey/white precipitates seen on
and within anterior lens capsule
3. Clear ring surrounded by circular
grey area when pupil is dilated
4. Made of amyloid material
- Amyloid and pigment released
Zonular rubbing causes shedding of iris
from iris rubbing against amyloid
pigment into aqueous and gets to TM
- Released into aqueous which is
then deposited into TM
TM becomes more pigmented (uneven),
Pigment is seen as darkly pigmented
but no amyloid seen in TM
band in filtration portion of TM confined
to relatively smooth bordered
circumscribed band
Pigment and amyloid deposited onto
Iris transillumination and Krukenbergs
corneal endo more inferiorly due to
spindles
convection currents (Krukenberg
spindles
Zonules usually weakened (on dilation,
IOP goes up)

3. Glaucoma associated with ocular trauma

Aet: Trauma can create tears in locations between sclera and uvea at corneo-scleral
junction > disruption of uveal meshwork and tears in TM, ciliary muscle and iris root
Clinical:
Gonioscope > small areas of irido-dialysis
Angle recession: Ciliary body band seen several times wider than TM (iris
pushed down into angle) > glaucoma can occur years later > check IOPs
annually
Hyphaema > indication of ocular trauma
Tx: 5 days bed rest with no weight lifting
4. Lens induced glaucoma:
Presentation:
Phacolytic glaucoma
Presents suddenly in eye with poor visual acuity and long-standing mature
cataract
Clinical:
Lens material leaks through incompetent anterior capsule > evokes
macrophage proliferation into anterior chamber
IOP increases due to macrophage and lens material physically blocking TM
Aet: Subluxated lens may block angle (Marfans syndrome and syphilis due to
weakened lens zonules)
Tx: First reduce inflammatory response, then surgically remove lens
5. Neovascular glaucoma:
Aet: Mostly due to rubeosis abnormal growth of blood vessels from retina; Occurs as
result of hypoxia to retina (not anoxia)
Risk factor: Diabetes, hypertension, retinal vessel occlusion (CRAO, BRAO, CRVO,
BRVO)
Clinical:
Small buds form in angle and pupil margin > grow out > weak, lack pericytes
and are fragile > tendency to bleed > formation of fibrovascular tissue >
contracts > push iris forward > synechiae like attachments > aqueous
drainage decreased
Tx: Laser; consider cause off hypoxia

RISK FACTORS FOR UVEITIS

- Age: 20-50; marked decrease after 70
- Sex:
a. Males: Ankylosing Spondylitis, Reiters syndrome, Behcets disease
b. Females: Sarcoid, Juvenile rheumatoid arthritis

COMMON AETIOLOGIES OF ANTERIOR UVEITIS

1. Idiopathic most common
2. Traumatic usually after corneal abrasion, FB or corneal insult
3. Infection H Simplex and Zoster; TB; syphilis; toxoplasmosis
4. Common systemic diseases:
a. Ankylosing spondylitis:
Prevalence Most common form of anterior uveitis; more in males
Hx
back pain > px progressively stoops over > abnormal sacro-iliac spine
radiographs
Dx
attack of anterior uveitis > acute > subsides within 4-6 weeks (mostly
uni)
Def
Immune complex disease
Blood Test
HLA B27 (HLA = human leucocyte antigen) > 98% +
b. Arthritis:
Def
Tests
Children

Ocular
involveme
nt
Presentati
on
Visual loss
Tx
Systemic
manifestat
ion

Known aetiology of anterior uveitis

Antinuclear antibody test (ANA) and RF factor
Stills disease/Juvenile chronic arthritis = special form of chronic
anterior uveitis affecting children
Subdivided into 3 on basis of joint pattern involvement
mostly seen in pauci-articular type;
mostly girls
Bilateral, white and painless eye
(4) band keratopathy glaucoma cataract macular oedema
Steroids
( 5) fever rash lymphadenopathy hepatosplenomegaly occasionally
cardiopulmonary involvement

c. Reiters syndrome:
Prevalence Men 20-40y
Ocular
(4) Acute anterior uveitis arthritis urethritis/dysentery sometimes
involveme conjunctivitis
nt
Presentati
Bilateral
on
Systemic
affects peripheral joints (knees)
manifestat
ion
Aetiology
May be related to chlamydial infection
Test
HLA B27 present

d. Ulcerative colitis:
Def
Inflammatory disease of distal colon and rectum
Aet
1. Crohns disease (inflammation of uvea and colon, and arthritis)
2. Behcets disease (Causes oral and genital ulcers blood test: HLA
B51)
3. Sarcoidosis (5% of all anterior uveitis; more associated with
posterior uveitis)

CLINICAL PRESENTATION
Most common symptoms:
1. Pain (sharp) often sudden onset
2. Blurred vision (slight) from corneal oedema or aqueous debris
3. Extreme photophobia
4. Tearing
5. Red eye
Most common signs:
1. Circumlimbal flush:
Vascular dilation and injection typically centred around peri-limbal conjunctival tissue;
grade of injection lessens posteriorly towards fornices
2. Blepharospasms:
Spasms of lid;
eye is uncomfortable, especially in bright lights;
difficulty keeping eyes open
3. Miotic pupil:
DT inflammation;
iris swells and pupil diameter is reduced;
doesnt always happen and pupil does still react
4. Inflammatory cells:
WBC (leucocytes, polymorphs, macrophages, lymphocytes);
cross vascular endothelium to float in aqueous;
high number > pus formed > hypopion
Cells circulate, agglutinate and become deposited on corneal endothelium > KP
Inflammatory cell finding NB in Dx of anterior uveitis
Observation difficult > can use slightly longer beam than conical
Cells graded 1-4:
1. No cells; Trace 1-3 cells
2. 4-10 cells
3. 15-20 cells
4. Too many to count
5. Most ever seen
5. Flare:
Sign of protein leakage from damaged iris BV
Sign of persisting vascular damage, especially after disappearance of cells
Shows as homogenous fog-like appearance in slit-lamp beam
Graded from 1-4; most severe when aqueous becomes fibrinoid

6. Keratic precipitates
Formation, see 4
Classic sign of uveitis
Found on corneal endothelium
Debris form sticky residue > convection pattern inferiorly on inferior cornea due to
currents and gravity
May disappear after Tx (steroids) or stay and pick up pigmentation
7. Synechiae:
a. Anterior: adhesion between cornea and iris
b. Posterior:Adhesion between iris and anterior lens
More likely to occur with anterior uveitis
Irregular pupil shape may result, especially under dilation
If iris is attached all the way around (to lens surface), aqueous will not circulate
normally > iris protrudes forward > iris bombe
8. Intra-ocular pressure:
Anterior uvea inflamed > shuts down ciliary body > pressure initially goes down (35mmHg) = first sign
Over time, floating debris blocks TM > secondary glaucoma
Steroid Tx may cause (iogenic) glaucoma
9. Iris nodules:
Accumulation of leucocytes on iris surface
Yellow-white
Usually associated with granulomatous uveitis or systemic disease
Two types:
1. Busacca nodules: larger; on surface of iris
2. Koeppe nodules: smaller; at pupil edge/margin

MANAGEMENT AND TREATMENT

How to prevent synechiae:
1. Keep pupil dilated and mobile use mydriatic/cycloplegic agents
With more intense inflammation, drugs less effective
2. Use parasympatholytic agents that work on iris sphincter (homatropine/cyclopentolate)
Calms ciliary body, prevents ciliary spasms causing pain and increases px comfort
How to prevent damage to iris BV:
1. Eliminate inflammation as quickly and completely as possible
Use strongest most effective topical steroid in frequent instillations
Steroids must be tapered as soon as possible
Prenisolone acetate 1%
2. Complications of steroids:
a. Increased IOP
b. Cataracts
c. Glaucoma

PHARMACEUTICAL APPLICATIONS
Use of diagnostic drugs in differentiation of pupil abnormalities
Refer to notes from Ocular Pharmacology in third year, particularly those on ocular antiinflammatory meds

PHARMACEUTICAL APPLICATION
Drugs used in management of posterior uveitis

Traditional management:
1. Topical or systemic corticosteroids
2. Cycloplegics
Severe uveitis unresponsive to steroids/ px with complications:
Immunosuppressants
First line therapy in px with Behcets disease involvinig posterior segment, Wegener
granulomatosis and necrotizing clerritis
Diseases are associated with systemic vasculitis, and treatment with
immunosuppressants can improve outcomes
Immunomodulatory therapy used where long-term Tx with systemic corticosteroids is
necessary:
1. Serpiginous choroiditis
2. Birdshot choroiditis
3. Vogt-Koyanagi Harada disease
4. Sympathetic ophthalmia
5. Juvenile idiopathic arthritis

VEGF
Full-length humanized anti-vascular endothelial growth factor monoclonal antibody
bevacizumab
Trerats refractory CME and neovascular complications of uveitis
Serial injections may be necessary and long-term tolerability and safety of med is
unknown
Tx of

refractory non-infectious uveitis:

Sustained release flucinolone implant (Retisert)
Approved by FDA
Released for 30 months
Allows tapering of systemic steroids and immunomodulatory agents
Cataract formation in phakic eyes
Risk of glaucomy 60%

Cycloplegics
Symptoms and complications of inflammation tempered with topical cycloplegics
Short-acting drops (cyclopentolate) and long-acting drops (atropine) used to:
1. decrease photophobia caused by ciliary spasm
2. break up/prevent formation of posterior synechiae

Corticosteroids
Uses:
1. Inhibit arachidonic acid release from phospholipids
2. Inhibit transcription and action of cytokines
3. Limits B- and T-cell activit
4. Indicated in inflammatory diseases of non-infectious cause
Routes of administration: (3) topical periocular systemic
Best route and dose determined for each patient
Minimum amount needed to control inflammation should be used to reduce
complications
Complications:
Serious adverse effects, esp with high doses and long-term use
Immunosuppressive agents commonly used for chronic or sight-threatening uveitis
A. Topical corticosteroids
Use: Anterior uveiis
Frequency: Depending on severity of inflammation, ranges from hourly to every other
day
Drug of choice: 1% prednisolone acetate (Precipitate > shake well before use)
Complication: May cause ocular hypertension > px monitored at 4-week to 6-week
intervals
B. Periocular corticosteroids
Use: When more posterior effect is necessary or when compliance is an issue
Route: Transseptal or sub-Tenon approach to deposit long-lasting steroid around eye
(deep transseptal injections may cause less ocuar hypertension than sub-Tenon)
Method: Initially treat px with topical steroid for 3-4 weeks prior to periocular to
identify steroid responding px
Complications: Not to be used in px with infectious uveitis or scleritis > scleral
thinning and possible perforation
Drug of choice: Triamcinolone acetonide
Triamcinolone
Uses:
1. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and
reversing capillary permeability
2. Used as intra-vitreal injection for retinal oedema
Immunosuppressive agents: 3 main categories of therapy:
1. Antimetabolites (3) azathioprine methotrexate mycophenolate mofetil
2. T-cell suppressors (2) cyclosporine - tacrolimus
3. Cytotoxic agents (2) cyclophosphamide chlorambucil
Alkylating agents

Most agents take several weeks to achieve efficacy, therefore initially used in conjunction
with oral corticosteroids
Once disease is under control, corticosteroids can be tapered

C. Systemic corticosteroids
Use: When systemic disease is present that also requires treatment, or for visionthreatening uveitis poorly responsible to other methods of delivery
Route: Oral or intravenous therapy
Complications: short-term and long-term adverse effects of corticosteroid use
considered
Drug of choice: Prednisone (oral)*
*Prednisolone (Pred Forte)
Uses:
1. Acute inflammations following eye surgery or other types of insults to eye
2. Decreases inflammation and corneal neovascularization
3. Suppresses migration of polymorphonuclear leukocytes
4. Reverses increased capillary permeability
5. Bacterial infections> concomitant use of anti-infective agents mandatory
Shake well before use