Viral Uveitis

7/29/2019 Viral Uveitis

1/33


2/33

Dr Anumeha


3/33

It includes:

Cmv retinitis

Human immunodeficiency virus uveitis

Progressive outer retinal necrosis

Acute retinal necrosis

Herpes-simplex uveitis

Varcilla zoster uveitis Congenital rubella


4/33

Pathogenesis :

Transmission occurs via infected bodyfluids, blood, or transplanted organs.

CMV can be found in blood, tissues,

saliva, vaginal secretions, semen, breastmilk, and urine


5/33

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.


6/33

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)


7/33

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


8/33

Non granular typeGranular type


9/33

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.


10/33

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


11/33

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


12/33

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


13/33

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.


14/33

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


15/33

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


16/33

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


17/33

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


18/33

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


19/33

T/t

Is difficult

But topical steroids and oralaciclovir(400mg five times the day ) havebeen used


20/33

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


21/33

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


22/33

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


23/33

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.


24/33

T/t

antiviral agent, acyclovir, is indicated when

posterior uveitis is progressive


25/33

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)


26/33

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


27/33

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


28/33

Investign and Mx:

PCR assay on vitreous samples

Mx :i/v ganciclovir alone or with foscarnet

intravitreal foscarnet


29/33

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


30/33

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


31/33

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.


32/33

salt and pepper fundus


33/33

Documents

Viral Uveitis