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8/3/2019 Uveal Tract- Dr Sison
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litianNotes 8
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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OphthalmologyMid Q2- Dr. Sison
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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OphthalmologyMid Q2- Dr. Sison
(+/-) 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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litianNotes 1
OphthalmologyMid Q2- Dr. Sison
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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OphthalmologyMid Q2- Dr. Sison
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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litianNotes 13
OphthalmologyMid Q2- Dr. Sison
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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OphthalmologyMid Q2- Dr. Sison
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