Good morning

Viral Uveitis
Dr Anumeha

It includes: Cmv retinitis Human immunodeficiency virus uveitis Progressive outer retinal necrosis Acute retinal necrosis Herpes-simplex uveitis Varcilla zoster uveitis Congenital rubella

Cmv retinitis
Pathogenesis : Transmission occurs via infected body fluids, blood, or transplanted organs. CMV can be found in blood, tissues, saliva, vaginal secretions, semen, breast milk, and urine

CLINICAL PRESENTATION 1) asymptomatic: peripheral lesions without significant vitreous inflammation can be detected 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 vitritis visual field defects Secondary rhegmatogenous retinal detachment may present with abrupt visual acuity or field loss.

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 retinal whitening, often associated with intraretinal hemorrhages and hard exudates --described

as "pizza pie" or "cheese pizza" or crumbled cheese and ketchup in appearance.

(This refers to large areas of dense opaque retina with blotchy intraretinal hemorrhages)

GRANULAR TYPE

: peripheral type of lesion

granular appearance with satellite lesions and less hemorrhage. Behind the advancing border is necrotic retina with mottled pigmentation from hyperplasia of the retinal pigment epithelium (RPE). The lesions progress in a brushfire manner, led by an active border. The rate of progression is typically slow Retinitis follows the nerve fiber layer. Retinitis produces wide areas of necrosis, scarring, and atrophy__ it is full thickness geographical necrotizing retinitis

Granular type

Non granular type

The area of retinal involvement divided into three concentric zones

zone 1 includes all of the retinal area within 2

DD 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 to the ampullae of the vortex veins, zone 3 is the retina peripheral to zone 2.
Zone 1 disease affects the macula, papillomacular bundle, or optic nerve and is therefore immediately vision threatening.

D/D Herpes zoster ophthalmicus herpes simplex keratitis, toxoplasmic retinochoroiditis, acute retinal necrosis, progressive outer retinal necrosis, syphilitic retinitis, Pneumocystis carinii choroiditis, Tuberculosis Candida Cryptococcus Lymphoma Vasculopathies (branch or central vein occlusions

Diagnosis
1) Accidental detection during OPD fundus examination 2) Complete blood count (CBC) with differential 3) CD4 count is a marker of immune dysfunction : CD4 >50 cells/mL - Little risk; screening examination every 6 months if CD4 50-100 cells/mL screen yearly if CD4 >100 cells/mL CD4 <50 cells/mL - Up to 35% incidence of CMV retinitis; median time to diagnosis of CMV retinitis is 13 months; screen every 3 months

4) PCR test can be qualitative or quantitative. Specimens can be obtained from serum, semen, or urine. Detection of CMV in the blood by DNA PCR is most predictive of developing CMV disease .

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 Pneumocystis pneumonia 6) Histopathologic : Large cells with eosinophilic intranuclear and/or intracytoplasmic inclusions (cytomegalo cells) typically are present. The intranuclear inclusions may have an owl eye appearance

Management Medical Surgical Medical Anti-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.

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 maintenance Valganciclovir: valine ester prodrug of ganciclovir. bioavailability is approximately 10 times higher A once-daily dose of 900?mg HAART (Highly active antiretroviral therapy) combination of two drug categories two or more reverse transcriptase inhibitors: zidovudine and

nevirapine
and one or more viral protease inhibitor: indinavir

or

ritonavir.
More effective IV route

Herpes simplex uveitis

Acquired primary infection is usually asymptomatic, although oral, skin, or eye lesions may sometimes be seen Symptoms in three ways: 1) Herpetic kerato-iridicyclitis 2) Herpetic iridocyclitis 3) Sympathetic herpetic uveitis

Herpetic kerato iridocyclitis: occurs as transient 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,more aqueous flare,medium sized KPs,hyphema is seen,post synechiae, sever pain aggravated by inc ocular tension

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 of dendritic ulcer and iridocyclitis
c/f acute and painful,aqueous flare,KPs and synechiae,iris atrophic patches

 Choroidal hemorrhage, vitreous opacities, retinal edema, and retinal vascular occlusions with ischemia can be seen Histologically, retinal necrosis and inflammatory cell infiltrates with intranuclear inclusion bodies are characteristic

widespread area of retinal necrosis

T/t
Is difficult But topical steroids and oral aciclovir(400mg five times the day ) have been used

Varicella zoster uveitis

Infection of eye from a congenital infection, primary infection, or reactivation In congenital varicellar syndrome, chorioretinal scars, similar to scars from toxoplasmosis infection, may be seen with hypoplastic discs and congenital cataract In primary acquired infection or with reactivation, active anterior or posterior uveitis can occur The uveitis is of two types: Diffuse exudative Inflammatory having localized eruptive lesions both are associated with severe neuralgic pain

Diffuse exudative type: May not be noticed due to lid swelling and trigeminal neuralgia This type is insidious and if undetected leads to post synachiae KPs are profound Some times hypopyon develops along with hyphema Sec glaucoma may develop.(but there is more tendency towards hypotony Iris atrophic pathes are there and sometimes hetrochromia may occur In severe cases globe shrinkage can occur and eye may have to be enucleated

Inflammatory type:
Eruptive lesions over iris resembling those of skin and cornea called as Herpes iridis Circumscribed swollen areas marked by active vascular dilatation along with hyphema Bleeding may be recurrent Violent iritis Small iris atrophic patches Sec glaucoma may develope

 Chorioretinal involvement is rare It can occur weeks or months after the initial skin disease. Severe patchy vasculitis and chorioretinitis can lead to focal retinal necrosis Occlusive vasculitis of the retina and choroid can lead to retinal artery occlusions and choroidal ischemia.

T/t antiviral agent, acyclovir, is indicated when posterior uveitis is progressive

Hiv retinitis
Hiv retinitis Hiv microangiopathy Hiv retinitis Signs: Ant uveitis and vitritis Small yellow white irregular lesions located in mid periphery and ant fundus t/t : anti retroviral therapy(not acvir and gancyclovir)

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 and spontaneously disappear

Progressive outer retinal necrosis

Usually occur in AIDS but can also occur in drug induced immunosuppression Cause: Varicella zoster virus which acts when there is immunosupression 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

Investign and Mx: PCR assay on vitreous samples Mx :i/v ganciclovir alone or with foscarnet intravitreal foscarnet

Congenital rubella
Transplacental transmission of virus during 3rd month of gestation Infection is postnatally or congenitally The postnatal infection may be asymptomatic or associated with fever, rash, and adenopathy. The eye is rarely involved

Congenital infection congenital rubella syndrome,is characterized by congenital heart disease, cataract, deafness, encephalitis, mental retardation, microphthalmia, corneal clouding, glaucoma, chorioretinitis, hepatosplenomegaly, and interstitial pneumonitis Ocular manifestations: o Ant uveitis : cause iris atrophy

o Retinopathy:
It may be unilateral or bilateral. Fine, granular, symmetric mottling of the pigment epithelium is seen in the periphery and post pole called as salt and pepper fundus pigment spicules and changes in the choroidal vasculature may be seen vision is usually not affected unless the patient develops subretinal neovascularization with disciform macular detachment, a possible late complication of the disease.

salt and pepper fundus

Thank you