2. Uvea =uveal layeruveal tractvascular
layer
It constitutes the midle vascular coat of eye
ball{grape shaped}
from anterior to posterior
iris ciliary body coroid
3.
4. Functions;
Nutrition and gas exchange
Light absorption=improves contrast of
retinal images by reducing reflected light
within eye{analogue to black paint inside
camera}
6. Anatomical
anterior
•Iris to pars plicata of cilaiary body
•Iritis,iridocyclitis
intermediate
•Pars plana and peripheral part of cilaiary body
posterior
•Involves choroid with or without retinal inflammation
•Choroiditis,corioretinitis,neuroretinitis
7. clinical
acute
•Sudden symptomatic onset
•Lasts for 6weeks to 3 months
chronic
• insidious and asymptomatic onset
•3months to years
recurrent
•Repeated episodes seperated by inactive
episodes of >3months with no treatement
10. Inflammation of uveal tissue is induced by
invasion of micro organisms.
It may be ,
Exogenous:infection directly gain entry into
eyes from outside.occurs following penetrating
injuries,perforation of corneal ulcer and
postoperatively .this causes suppurative irido
cyclitis which turns to endophthalmitis
Secondary:from the neighbouring structures
Example:keratitis,retinitis
Endogenous:through the blood stream.this
plays important role in inflammation of uvea
11. I. Suppurative:by direct invasion of pathogen
into uveal tissue
II. Non suppurative:involves uveitogenic
processes such as,
Due to hypersensitivity reation:to the protein
and toxin causes antigen antibody reaction.
Microbial induced autoimmune uveitis:
Molecular micmicry;cross rxn of
Microbial antigens
Stimulation of innate immunity:autoimmunity
following the stimulation with microbial
products.eg:bacterial DNA,viral RNA
12. Uveitis induced by bacterial exotoxins and
other secretory products:hemolysin,alpha
toxin,collagenases.
Microbial cellwall stimulated alternate
pathway for inflammation:complementary
system,C reactive protein
16. Routine investigation of uveitis:
o Carefull history taking,detailed ocular
examination,intraocular pressure,slit lamp
examination,fundus examination after
dilating pupil.
o Haematological investigation
o Urine examination
o Stool examination
o Radiological investigation
o Skin tests
17.
18. Types:
Uveitis in chronic systemic bacterial infections:
Tubercular Uveitis:chronic granulomatous infection by
bovine or human tubercle bacilli
Accounts for 1%of uveitis
Clinical presentation:
Tubercular anterior uveitis:ocurs as
multiple miliary tubercles on choroid appears as round
yellow white nodules 1/6-1/2 disc in size.associated
with tubercular meningitis.
Douse or multifocal choroiditis
Choroidal granuloma
Vasculitis[eales disease]
19.
20. Diagnosis:
postive skin test
Associated systemic tuberculosis findings
Positive response to isoniazid test[300mg OD
for 3 days]
Treatement:chemoterapy with rifamicin and
isoniazid for 12 months
Treatement for uveitis
21. leprotic uveitis:hansen disease
Clinical types:
o Acute iritis by ag-ab deposition,leads to
severe exudation reaction
o Chronic granulomatous iritis due to direct
organism invasion,charecterised by the
presence of iris pearl near pupillary margins
in neclace form,coalesce of small pearls to
form larger once.
Treatement:dapsone 50-100mg+local theray of
iridocyclitis
22. Spirochetetial uveitis:
>Acquired syphylitic uveitis; chronic veneral infection
caused by TREPONEMA
PALLIDUM{spirochaete}.affects both anterior and
posterior uvea.
o syphilitic anterior uveitis:occurs as acute plastic iritis
or granulomatous iritis
Acute plastic iritis occurs as secondary stage of syphilis
also as herxheimer rxn 24-48 hrs of penicillin dose.
Gummatous anterior uveitis late in secondary or
tertiary stage of syphilis .forms yellowish red highly
vascularised multiple nodules arranged near the
pupillary border.
23.
24. o Syphilitic posterior uveitis; occurs as
disseminated peripheral or diffuse
choroiditis.
Clinical diagnosis:confirmed by FTA-ABSblood
test,more specific and sensitive than TPI and
VDRL
Treatement:systemic penicillin or other anti
syphilitic drugs
Local therapy of uveitis
25. Parasitic uveitis :
toxoplasmosis:protozoan infestation caused by
TOXOPLASMA GONDII .primarily affects CNS.systemic
lesion are more marked in immunocompromised patient.
Most common cause of posterior uveitis accounts for 90%
of focal necrotising retinitis.
Clinical presntation: 3 forms
Congenial toxoplasmosis :more common ,acquired by
the fetus through transplacental route during
pregnancy.49%are born with either active or inactive
form.most of them born with inactive
disease,characterised by bilateral healed punched out
heavily pigmented chorioretinal scars in macular
area.discoverd when child is brought for defective vision
or squint.
26.
27. Acquired toxoplasmosis:infestation is
acquired by eating the under cooked meat
of intermediate host containing cyst from
the parasite.lesions are similar to congenital
one added with punctate outer retinal
toxoplasmosis.
28. Recurrent toxoplasmic retinochoroiditis:
Pathogenesis: Parasite in fetus through
transplacental route
involving retina and brain
Excite ab formation. after
healing of lesion,parasite
remain encysted in
inactive form
After 10-40 yrs cyst rupture
and release hundreds of
parasite,adjacent to old
inactive pigmented scar
29. Features:whitish yellow slightly raised area of
infiltration located near margins of old
punched out scarred lesion in macula ,radial
pigmentation with necrosis in the centre
with severe vitritis.
Diagnosis by IFA,HA,ELISA. treatement by
topical and systemic steroids
+spiramycin/clindamycin
30. Toxocariasis:caused by TOXOCARA CANIS
Ocular toxocariasis is always unilateral and presents
as,
1. Toxocara chronic endophthalmitis with leucocoria
due to marked vitrious clouding.mimics
retinoblastoma and seen in 2-10 yrs.
2. Posterior pole granuloma:yellow white solitary
raised nodule affecting unilateral vision
3. Peripheral granuloma:assosiated with vitreous
band formation.
Daignosis by ELISA BLOOD TEST.treatement consiss of
periocular injection of steroids and systemic.pars
plana vitrectomy is also done.
31.
32. Fungal uveitis:
o Presumed ocular histoplasmosis syndrome:caused by
HISTOPLASMA CAPSULATUM.
Features:
1) histo spots,atrophic spots scattered in mid retinal
periphery.roundish yellowish white lesion .begins to
appear in early childhood.
2) Macular lesions starts as atrophic macular scar, a hole
in bruchs membrane sub retinal choroidal
neovascularisation leakage of fluid serous
detachment complicated by haemorrhages repeatedly
later forms fibrous disciform scar.
Daignosis by +ve histoplasmin skin test and CFT.FA inearly
diagnosis.treatement by laser photo coagulation of
subretinal neovascular membrane.
33. o Candidiasis:CANDIDA ALBICANS in
immunocompromised patients.
Ocular candidiasis:
1) Anterior uveitis with hypopyon
2) Multifocal chorioretinitis:roth’s spots
3) Candida endophthalmitis:puff/cotton
ball,string of pearls
Treatement :topical cycloplegics+antifungals
systemic antifungals
pars plana vitrectomy
34.
35. Viral uveitis:
Herpeszooster ophthalmicus:involvement of
fifth nerve by VZV,causes non
granulomatous iridocyclitis.complicated by
iris atrophy and secondary glaucoma.
Herpes simplex uveitis:forming dendritic or
geographical corneal ulcers with disciform
keratitis.
Treated by topical
steroids,cycloplegics,systemic acyclovir
36. CMV retinitis:occurs only en CD4 count,50 cells/mm3.
Features:
Symptoms.oten asymptomatic,some presents with
scotoma/floaters/decresed vision.
Signs:anterior segment usually rare.
Posterior include,
haemorrhagic retinitis with necrosis{pizza pie
appearance}.
Granular retinitis
Complications including RD, retinal atrophy,optic nerve
disease.
Treated bt HAART+anti-CMV drugs.
37.
38. Acute retinal necrosis:caused by
VZV{commom},HSV1and 2,CMV
Features:
Symptoms.pain,photophobia,floaters,ocular
discomfort,decresed visual acuity.
Signs:ant segment may or may not show
inflammation in AC
Marked vitritis
Retinal lesions
Treatement:,systemic antivirals{lifelong},Systemic
steriods,aspirin,barrier laser
photocoagulation,vitrectmy with silicon oil
injection.
39. Progressive outer retinal necrosis:rare
devastating retinal necrosis caused by VZV
in immunocompromised persons.
Features:
Painless loss of vision
Retinal lesions with rapid coalese white areas.
RD common complication.
Treatement:IV gancyclovir/foscarnet+intra
vitreal gancyclovir.
