Uveal Tract- Dr Sison

8/3/2019 Uveal Tract- Dr Sison

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OphthalmologyMid Q2- Dr. Sison

Uveal Tract: Iris, Ciliary Body, Choroid

Anatomy & Physiology

middle vascular layer of the eye

Iris is the anterior most portion of the uvea (red) Ciliary body (yellow) Then posteriorly, is your choroid

A. Iris

Divides the aqueous compartment contains the pupil, sphincter dilator pupillae muscles.

Is the pigmented structure that divides the anterior andposterior chamber, divides the aqueous compartment

Contains the pupil which is used to regulate the amountof light entering the eye

Spincter located near the pupilary margin area andcontains the dilator pupillae to make the pupil wider

Sphincter pupillae muscle is parasympathetic Dilateor pupillae muscle is sympathetic

B. CiliaryBody

posterior extension of iris contains the ciliary muscle

responsible for accomodation outer pigmented layer is continuous

posteriorly with RPE

thats not important inner non-pigmented layer extends

posteriorly to become sensory retina,

produces aqueous humor

What is important is that (1)it contains the ciliarymuscle for accommodation (2) it contains an inner

pigmented layer which produces your aqueous humor

Remember it is the non-pigmented layer that producesit

Ill ask 2 questions here

Aqueous Humor

contributes to maintenance of IOP support metabolism of cornea and lens composition similar to plasma with nearly all protein

removed

Basic difference is there is a very low oralmost no protein content in Aqueous

Clinical significance: in cases of inflammationin the anterior chamber, there is an increase

in protein content in aqueous abnormal,

remember that

Produced by the non-pigmented epithelium of ciliarybody

Accomodation

function of both the radial and longitudinal muscles inbetween is the oblique muscle

contraction leads to relaxation of tension on lenscapsule assuming a more spherical shape thus

increasing refractive power to focus close objects

relaxation leads to the reverseC. Choroid

major portion of the uvea vascular supply of outer half of the retina composed primarily of:

1. choriocapillaries supplies the outer half of the retina

2. medium vessels (veins)3. outer large vessels

BLOOD SUPPLY and INNERVATION

anterior uvea is supplied by long posterior ciliaryarteries, posteriorly by the short ciliary arteries

Bruchs membrane: basement membrane Nerve supply: short posterior and long anterior ciliary

nerves


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UVEITIS

If the iris is mainly affected, we call it as anterior uveitisor iritis,

Intermediate or cilitis Choroiditis or Posterior uveitis When all 3 components are affectedpanuveitis Inflammation of iris and ciliary bodyusually base it

on the most prominent structure that has more

inflammation, so if in iris, it is still called anterior uveitis

I. ACUTE ANTERIOR UVEITISSigns and symptoms (Non-granulomatous type)

Acute onset with ocular pain Comes from spasm of iris sphincter and spasm of

ciliary body

Ciliary congestion Redness around the cornea, just around the

limbal area

Photophobia Spasm in sphincter and ciliary muscle, everytime

there is light, your pupil constricts, when it

constricts, there is pain elicited because the

sphincter is also inflammed

Blurred vision Because of anterior chamber flare and cell

Fine KPs (keratic precipitates) on endothelium & T.M.(trabecular meshwork

KP: white blood cells or leukocytes that haveprecipitates in the endothelial layer of cornea,precipiates in the cornea

Pupil is miotic Spasm of sphincter pupillae muscle

(+) AC flare/cell, + or fibrin exudation Anterior chamber flare is a sign that there is an increase

in protein content in aqueous so it will appear turbid

seen as anterior chamber flare

Presence of cells (RBC or WBC) in anterior chamber isindicative of uveitis

If too much protein content, you can have fibrinexudation synechiae between iris and lens

posterior synechiae (adhesion)

+ or posterior synechiae Course of disease is acute

Prognosis is good but recurrence is common

Ciliary congestion: perilimbal inflammation

Fine white keratic precipitates

Keratin precipitates WBC which sticks to posterior surface of the cornea are

called keratin precipitates

If keratin precipitates are pigmented, it meansinflammation is recent

If non-pigmented, inflammation is old

AC flare

This is how the flare looks like when you use the slitlamp

White structure is cornea Lens If you shine a beam of light and no protein or cell

content, cant see any flare

In cases where protein content is increaseddisperse the lightanterior chamber flare

indicative of increased protein in the aqueous

Flare

Lens

Cornea


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(+/-) fibrin exudation

If a lot of WBC in anterior chamber, it will form ameniscus level (sa baba) and the presence of gross WBC

in the anterior chamber is what we call hypopyon

If you see cells in the anterior chamber, these aremicroscopic WBC

Once it becomes macroscopic, it becomes hypopyon,white structure is pus in the anterior chamber, looking

upwards, whitish structure over the lens fibrin

exudate

II. INTERMEDIATE UVEITIS Aka Pars planitis or chronic cyclitis Presents as floaters

III. POSTERIOR UVEITIS Limited to the posterior segment

Any structure behind lens and ciliary body Granulomatous type more commonly seen Insidious onset, no pain, minimal photophobia

Why no pain? Because there is no muscle No iris sphincterminimal photophobia

Choroidal lesions usually seen as focal patchy areas ofinfiltrate

Associated with vitritis and retinitis Also affects choroid and retina

IV. PANUVEITIS Involves the entire uvea

Differential Diagnoses of Uveitis

a. Conjunctivitis Entire bulbar conjunctiva is hyperemic or

congested

Increase tearing and possible mucopurulentdischarge

b. Acute angle closure glaucoma Difference between acute anterior uveitis is

the pressure in glaucoma is elevated, in AAU,

IOP is normal

Pupil in AAU is miotic, in AACG is dilatedc. Retinoblastoma pseudohypopyon

There is pseudohypopyon meaning thepresence of a whitish material with meniscus

level in anterior chamber, these are tumor

cells pseudohypopyon

Ultrasound: detect presence of a tumor in theposterior segment in retinoblastoma, in

uveitis, no tumor seen

d. Juvenile xanthogranuloma hyphemae. Pseudoexfoliation of the lens

Take note of the first three In acute anterior uveitis ciliary injection, no tearing and

associated discharge

Hypopyon


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NON-SPECIFIC TREATMENT OF UVEITIS

A. CORTICOSTEROIDS MC used1. Topical preparations

a. Dexamethasone PO4b. Dexamethasone ROHc. Prednisolone acetated. Prednisolone PO4e. Fluorometholone

NB: drops are more effective than ointment

preparation

Dexamethasone is the most potent, least potent isfluorometholone

Steroid induced glaucoma elevation in IOP Give fluorometholone causes the least

elevation in IOP

I will ask which is the most potent and has theleast effect on the IOP

2. Systemic Cotrticosteroids If after periocular injection of steroids and

inflammation is not yet controlledsystemic

corticosteroids

Used in tractable anterior uveitis notresponding to topical drops alone or in

posterior or panuveitis

Short acting Cortisone Prednisone Prednisolone Methylprednisolone

Intermediate acting Paramethasone Triamcinolone

Long acting Dexamethasone Betamethasone Metamethasone

Of the steroids, our favorite is ourprednisone,dexamethasone ormethylprednisolone, these

are the 3 MC steroids that we use

You dont have to memorize all of these3. Periocular injection Depomethylprednisolone 40-80 mg once every 2 weeks If topical steroids are not enough in controlling

the inflammatory reaction, we give periocular

injection, we inject the steroids

subconjunctival and usually we give

methylprednisolone ortriamcinolone

Major advantage: Long lasting effectonceevery 2 weeks

Major disadvantage: elevation of IOP insteroid responders

Drops: every hour round the clock

B. MYDRIATICS CYCLOPLEGICS Relieve iris sphincter and ciliary muscle spasm Prevent posterior synechiae

Atropine 1-4% Homatropine 5% Cyclopentolate 1%

NB: longest acting is atropine (up to 2 weeks);Shorter cyclopentolate

Much shorter tropicamide

MOA: Paralyzes sphincter muscles to relieveof pain

Symptomatic (pain) To prevent posterior synechiae:

adhesion between iris and lens

In cases of anterior uveitis, there is a tendencyfor the iris to adhere to the lens posterior

synechiae

Cycloplegics prevent synechiae

C. IMMUNOSUPPRESSIVE AGENTS Used in concert with an oncologist or

hematologist

For other diseases with uveitisD. NSAIDS

Steroid responders: increase in IOP with theprolonged use of steroids

In these cases, NSAIDs are given SE: GI irritation and nephrotoxicity (long

term use)

1.Salicylates2.Phenylbutazone3.Anti-prostaglandin drugs (naproxen)

DOC in controlling inflammatory process MC short term effect: GI irritation Long term effect: nephrotoxic

E. PHOTOCOAGULATION The use of laser for ocular histoplasmosis Treatment of choice in POH when subretinal

neovascularization develops


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COMPLICATIONS OF UVEITIS

A. Band Keratopathy Complication of anterior uveitis Calcified opacity at level ofBowmans layer Cornea becomes opaque vision is disrupted May be removed for visual or cosmetic reasons by

using chelating agents (EDTA)

There is a haze of calcium deposits as pointed by the arrows

B. Cataracts 2nd MC complication Usually (but not always) a complication of chronic

steroid use

Posterior subcapsularC. Macular surface wrinkling

In cases of uveitis, the IOP is usually low, when it isvery low, there would be wrinkling of the macula

Pic of BK: cant see pupil clearly because there is ahaze of calcium deposites as pointed by the arrows

D. Edema of disk and macula Usually seen in posterior and panuveitis

E. Corneal edema Happens because of secondary glaucoma In uveitis when there is posterior synechiae, the

aqueous humor outflow is obstructed IOPincreases

This results in corneal edemaF. Secondary glaucoma

If you have posterior synechiae and your aqueousfrom posterior chamber cant pass through pupil

build of up pressure increase in IOP (glaucoma)

corneal edema

G. Retinal detachment May be EXUDATIVE as in VKH syndrome

Normally the pupil is round; if it is not then it suggests a previous

attack of uveitis; 360 degrees of synechiae for IOP to increase.

ETIOLOGY: Posterior Uveitis

1. Infectious disorders Viruses Bacteria Fungi Parasitic

2. Non-infectious disorders Auto-immune Malignancy Unknown etiology All of the above!

A. OCULAR TOXOPLASMOSIS Caused by Toxoplasma gondii Most common cause of chorioretinitis and posterior

uveitis

Definitive host: cat It enters the human body upon contact with the feces

of the cat (fecal-oral)

Presentation Floaters : WBC and pus cells in vitreous Photophobia Blurring of vision if the macula is affected

Ocular lesions: FOCAL chorioretinitis Sharp borders with pigmented borders

Blurring of vision if macula is affected

A. Recurrent toxoplasmic retinochoroiditis: Funduscopy is unclear

Why is it not clear? Because vitreous is hazy because of thepresence of pus cells

If inflammatory process has cleared of, you will see areas ofscars in your fundus

Can see retinal scars brought about by old chorioretinitis

TREATMENT: Ocular Toxoplasmosis

1. Pyrimethamine 25mg OD plus sulfadiazine 0.5-1 gmQID x 4wks

2. Photocoagulation** - in cases of neovascularization3. Cryotherapy** - in cases of neovascularization4. Steroids*


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PROGNOSIS is good if the macula is not affected; but once

macula is affected, you cant restore lost vision

B. OCULAR TOXOCARIASIS Caused by intestinal parasites (cat / dogs) Usually unilateral Redness, blurring, whitish pupil Fundus: focal whitish GRANULOMA (+/-) iridocyclytis / cataract May also have simultaneous anterior uveitis What are the causes of white pupil? Toxocara,

retinoblastoma

You can also have anterior uveitis but labeled asposterior

Pic: What you see here, nerve, blood vessels, whitelesions it the granuloma, inside it is your parasite

What will happen if you laser theparasite? The lysis of the body willcause more inflammatory reaction

Causes of white pupil (leucocoria):

Retinoblastoma Toxocara

Cataract

** If you do lLaser of the parasite: there will be more

inflammatory reaction; the granuloma is a protective mechanism

of the body

Laboratory findings

Titer of 1:8 for T. canis antibodies

Treatment

1. Systemic / periocular steroids2. Vitrectomy for severe vitamin fibrosis remove the granuloma including the parasite by

removing a part of the vitreous

** Intraocular inflammation is aggravated by death& disintegration of the parasite

ACQUIRED IMMUNODEFICIENCY SYNDROME

Ocular manifestations include:

COTTON WOOL spots Indicative of ischemia

Retinal HEMORRHAGES There is no error of refraction Infections from opportunistic organisms MC due to CMV

You see here several cotton wool spots

DDx for cotton wool spots: SLE

Hemorrhages and cotton wool spots

NB:cotton wool spots are indicative of ischemia

DIFFUSE UVEITIS

Sympathetic ophthalmia

Usually a panuveitis There isn exciting eye and a sympathizing eye E.g. The R eye is injured, after the L eye will also

develop uveitis

The good eye will have a granulomatou type ofuveitis as early as 10 days from the injury of the bad

eye

Bilateral granulomatous uveitis


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Probably due to hypersensitivity to pigment-bearingcells in the uvea

Occurs as early as 10 days after perforating injury orfollowing retained foreign bodies

Injured (exciting) eye becomes inflamed first What to do? Remove the severely injured eye before

the other eye develops uveitis

Signs and symptoms

Photophobia, REDNESS, blurring in the sympathizingeye

Treatment

For a severely injured sightless eye enucleation within10 days after trauma

Give steroids!!Wonder drug of uveitis

BENIGN TUMORS

Iris nevus

Flat benign tumor arising from melanocytic cells fromthe neural crest

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Uveal Tract- Dr Sison