Download - Viral Uveitis
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Dr Anumeha
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It includes:
Cmv retinitis
Human immunodeficiency virus uveitis
Progressive outer retinal necrosis
Acute retinal necrosis
Herpes-simplex uveitis
Varcilla zoster uveitis Congenital rubella
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Pathogenesis :
Transmission occurs via infected bodyfluids, blood, or transplanted organs.
CMV can be found in blood, tissues,
saliva, vaginal secretions, semen, breastmilk, and urine
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CLINICAL PRESENTATION
1) asymptomatic:
peripheral lesions without significant vitreous inflammation can bedetected incidentally in routine examination
2) Symptomatic:
Floaters (spots, bugs, spider webs)
Light flashes metamorphopsia Blind spots Blurred vision Obstructed areas of vision Sudden diminuation of vision
vitritisvisual field defects
Secondary rhegmatogenous retinal detachment may present with abruptvisual acuity or field loss.
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Varients of the disease: (based on morphology)
Stages
NON GRANULAR TYPE: (hemorrhagic type)More common.
The disease progresses along the retinal blood
vessels, causing confluent areas of retinalwhitening, often associated with intraretinalhemorrhages and hard exudates --describedas "pizza pie" or "cheese pizza" or crumbled cheese and ketchup in
appearance.(This refers to large areas of dense opaqueretina with blotchy intraretinal hemorrhages)
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GRANULAR TYPE : peripheral type of lesion
granular appearance with satellite lesions and lesshemorrhage.
Behind the advancing border is necrotic retina withmottled pigmentation from hyperplasia of the retinalpigment epithelium (RPE).
The lesions progress in a brushfire manner, led byan active border. The rate of progression is typically slow
Retinitis follows the nerve fiber layer.
Retinitis produces wide areas of necrosis, scarring, andatrophy__it is full thickness geographical necrotizingretinitis
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Non granular typeGranular type
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The area of retinal involvement divided into threeconcentric zones
zone 1 includes all of the retinal area within 2DD of the center of the macula or within 1 DD of
the margin of the optic disc
Zone 2 extends from the borders of zone 1 tothe ampullae of the vortex veins,
zone 3 is the retina peripheral to zone 2.
Zone 1 disease affects the macula, papillomacularbundle, or optic nerve and is therefore immediatelyvision threatening.
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D/D Herpes zoster ophthalmicus herpes simplex keratitis,
toxoplasmic retinochoroiditis, acute retinal necrosis, progressive outer retinal necrosis, syphilitic retinitis, Pneumocystis cariniichoroiditis, Tuberculosis Candida
Cryptococcus Lymphoma Vasculopathies (branch or central vein
occlusions
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Diagnosis1) Accidental detection during OPD fundus examination2) Complete blood count (CBC) with differential
3) CD4 count is a marker of immune dysfunction :
CD4 >50 cells/mL - Little risk; screening examinationevery 6 months if CD4 50-100 cells/mL
screen yearly if CD4 >100 cells/mL
CD4
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5) Imaging Studies Ultrasound is used for evaluation of retinal
detachment, particularly if vitritis obscures
adequate fundus visualization. Fluorescein angiogram - Assessment for areas
of ischemia Chest x-ray - Assessment for concurrent
Pneumocystispneumonia
6) Histopathologic : Large cells with eosinophilicintranuclear and/or intracytoplasmic inclusions(cytomegalo cells) typically are present. Theintranuclear inclusions may have an owl eyeappearance
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Management Medical Surgical
MedicalAnti-CMV Drugs:
Ganciclovir: nucleoside analog
as intravenous infusion, oral therapy, and as an intravitreal,sustained-release implant. It is virostatic against CMV. IV dose: (5 mg/kg BD) for 2-3 weeks then then OD daily at a
maintenance dose of 5 mg/kg/day. injected intravitreally, using doses of 2002000 g once to twice
weekly. Oral ganciclovir : low bioavailability has to be taken in high doses
(30004500mg daily). intravitreal, sustained-release implant: releases drug 1 g per hour.
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Foscarnet sodium: pyrophosphate analog IV dose: 90 mg/kg twice a day,maintainance:are 90 or 120
mg/kg/day OD intravitreally, at a dose of 1.22.4 mg once or twice a week.
Cidofovir: nucleoside analogue IV: 5mg/kg once weekly and once every 2 weeks for induction and
maintenanceValganciclovir: valine ester prodrug of ganciclovir.bioavailability is approximately 10 times higherA once-daily dose of 900?mg
HAART (Highly active antiretroviral therapy) combination of two drug categories
two or more reverse transcriptase inhibitors: zidovudine andnevirapine
and one or more viral protease inhibitor: indinavir orritonavir.
More effective IV route
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Acquired primary infection is usually
asymptomatic, although oral, skin, or eyelesions may sometimes be seen
Symptoms in three ways:
1) Herpetic kerato-iridicyclitis
2) Herpetic iridocyclitis3) Sympathetic herpetic uveitis
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Herpetic kerato iridocyclitis: occurs astransient and is self limited.
s/s : mild ciliray flush few cells in aqueous with out KPs
it is invariable continuation of dendritic
keratitis and subsides with corneal lesion.If disciform keratitis develops then uveitis
is severe: marked ciliary injection,moreaqueous flare,medium sizedKPs,hyphema is seen,post synechiae,sever pain aggravated by inc oculartension
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Herpitic iridocyclitis:
Due to presence of virus in uvea itself
Virus may remains latent for many months
in cornea aft healing of herpetic ulcer
Reactivation causes recurrence ofdendritic ulcer and iridocyclitis
c/f acute and painful,aqueous flare,KPs
and synechiae,iris atrophic patches
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Choroidal hemorrhage, vitreous opacities, retinal edema,and retinal vascular occlusions with ischemia can beseen
Histologically, retinal necrosis and inflammatory cellinfiltrates with intranuclear inclusion bodies arecharacteristic
widespread area of retinal necrosis
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T/t
Is difficult
But topical steroids and oralaciclovir(400mg five times the day ) havebeen used
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Infection of eye from a congenital infection, primaryinfection, or reactivation
In congenital varicellar syndrome, chorioretinal scars,similar to scars from toxoplasmosis infection, may beseen with hypoplastic discs and congenital cataract
In primary acquired infection or with reactivation, activeanterior or posterior uveitis can occur
The uveitis is of two types:
Diffuse exudative Inflammatory having localized eruptive lesionsboth are associated with severe neuralgic pain
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Diffuse exudative type:
May not be noticed due to lid swelling and trigeminalneuralgia
This type is insidious and if undetected leads to postsynachiae
KPs are profound
Some times hypopyon develops along with hyphema
Sec glaucoma may develop.(but there is more tendencytowards hypotony
Iris atrophic pathes are there and sometimeshetrochromia may occur
In severe cases globe shrinkage can occur and eye mayhave to be enucleated
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Inflammatory type: Eruptive lesions over iris resembling those of
skin and cornea called as Herpes iridis
Circumscribed swollen areas marked by activevascular dilatation along with hyphema
Bleeding may be recurrent Violent iritis
Small iris atrophic patches
Sec glaucoma may develope
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Chorioretinal involvement is rare
It can occur weeks or months after the
initial skin disease. Severe patchyvasculitis and chorioretinitis can lead tofocal retinal necrosis
Occlusive vasculitis of the retina andchoroid can lead to retinal arteryocclusions and choroidal ischemia.
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T/t
antiviral agent, acyclovir, is indicated when
posterior uveitis is progressive
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Hiv retinitis Hiv microangiopathy
Hiv retinitisSigns: Ant uveitis and vitritis Small yellow white irregular lesions located in
mid periphery and ant fundust/t : anti retroviral therapy(not acvir andgancyclovir)
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Hiv microangiopathy
Develops in 70% of pts with decilining
CD4+count Causes:
Immune complex deposition
HIV infection of retinal vascular endothelium
Hage abnormalities
abnormal retinal hemodynamics
Signs:
Cotton wool spots with retinal hages
Lesions are usually asymptomatic andspontaneously disappear
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Usually occur in AIDS but can also occur in drug inducedimmunosuppression
Cause:
Varicella zoster virus which acts when there isimmunosupression
S/S Progressive vision loss which is unilateral initially
Minimal ant uveitis
Multifocal yellow white retinal infiltrates with min viritis
Early macular involvment Rapid full thickness retinal necrosis
Vit inflamm is late & shows extensive retinal necrosis
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Investign and Mx:
PCR assay on vitreous samples
Mx :i/v ganciclovir alone or with foscarnet
intravitreal foscarnet
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Congenital rubella
Transplacental transmission of virus during
3rd month of gestation
Infection is postnatally or congenitally
The postnatal infection may beasymptomatic or associated with fever,rash, and adenopathy. The eye is rarely
involved
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Congenital infection
congenital rubella syndrome,is characterized
by congenital heart disease, cataract,deafness, encephalitis, mental retardation,microphthalmia, corneal clouding,
glaucoma, chorioretinitis,hepatosplenomegaly, and interstitialpneumonitis
Ocular manifestations:o Ant uveitis : cause iris atrophy
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o Retinopathy:
It may be unilateral or bilateral. Fine, granular,
symmetric mottling of the pigment epithelium isseen in the periphery and post pole called assalt and pepper fundus
pigment spicules and changes in the choroidalvasculature may be seen
vision is usually not affected unless the patientdevelops subretinal neovascularization with
disciform macular detachment, a possible latecomplication of the disease.
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salt and pepper fundus
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