HERPETIC VIRAL RETINITIS

1. HERPETIC VIRAL RETINITIS
Dr Shruti Laddha

2. ARN SYNDROME
• Acute primarily peripheral, necrotizing retinitis, retinal arteriolitis and mild to severe
vitritis.
• Usually unilateral
• Caused by – HSV, HZV, CMV
• Immunocompetent
Clinical characteritics –
• focal, well-demarcated areas of retinal necrosis located in the peripheral retina,
• rapid, circumferential progression of necrosis,
• evidence of occlusive vasculopathy
• prominent inflammatory reaction in the vitreous and anterior chamber.

3. Other features-
• Disc edema
• Granulomatous anterior uveitis with secondary glaucoma
• Exudative RD
• Rhegmatogenous RD

4. PROGRESSIVE OUTER RETINITAL NECROSIS
• Forster et al.
• Immunocompromised
• Minimal nongranulomatous anterior uveitis
• No vitritis
• Necrotizing retinitis
• Starting at the posterior pole and spreading toward the peripheral retina.
• Foci of lesions become rapidly confluent and involve the entire retina
• Unlike ARN syndrome, retinal vasculitis and optic neuritis are less common, but
retinitis is often bilateral.
• RD may occur

5. Extensive confluent retinal whitening,
retinal exudation, intraretinal
hemorrhage, consistent with infectious
retinitis such as progressive outer
retinal necrosis (PORN). • retinal vasculature is minimally involved, at leastinitially
• Perivascular clearing of the retinal opacification is characteristic of
PORN syndrome

7. CYTOMEGALOVIRUS RETINITIS
• Immunocompromised- HIV patients
• CD4 lymphocytes 50-100/mm3
• passage of the virus across the blood retinal barrier, when local defense
mechanisms are almost completely abolished.
• Viral progression into the retina seems to occur in a polarized manner(inner to
outer)---
internal blood-retinal barrier is disrupted after primary replication in endothelial cells
viral particles to reach retinal glial cells.
CMV then spreads towards the retinal pigment epithelium

8. • Systematic fundus examination should be performed every 3 months if CD4
lymphocytes counts are below 50/mm3.
• Few cases - CMV retinitis – immunocompetent patients after intravitreal injection of
Triamcinolone or after Fluocinolone acetonide implant.
• White fluffy areas of necrotizing retinitis associated with hemorrhages and vascular
sheating.
• Early CMV retinitis may begin with a small, white retinal infiltrate.
• The lesion may masquerade as a cotton-wool spot present in HIV-related
microvasculopathy.

9. Two subtypes of CMV retinitis
Fulminant or Edematous variant
Dense, white confluent opacifications
of the retina without any central atrophic
lesion occur usually along vessels, associated
with retinal hemorrhages and inflammatory
vascular sheating.
Indolent or Granular variant of disease associates
granular foci of retinal necrosis with a central atrophic
zone, fewer hemorrhages and less vascular sheating.
Papillitis may occur. Border of retinal necrosis is usually
irregular in both variants, surrounded by satellite
infiltrates.

10. • Slow progression
• Destruction of the entire retina occurs within 3 to 6 months in the absence of
anti-CMV therapy.
• Cicatricial lesions –atrophic retina with vessel rarefaction
T/T
• Anti viral, ART
• maintainance anti-CMV therapy to be continued till CD4 increase

11. Non-necrotizing Herpetic Retinopathies
(NNHR)
• Molecular analysis applied to ocular fluids confirmed the presence of herpes virus
DNA in patients presenting with different forms of chronic and atypical posterior
uveitis, such as Behçet disease, retinal vasculitis and birdshot retinochoroidopathy .
• May be associated with hemmorhages
• Generally bilateral
• Pt is generally steroid resistant or steroid dependent at high dose.
FFA-papillitis, retinal vasculitis and cystoid
macular edema in a case of HHV-8-associated
nonnecrotic herpetic retinopathy

12. • Children-acute retinochoroiditis with diffuse hemorrhages
• Adults - chronic choroiditis or vasculitis
• PCR-based assays – herpes viral etiology in 13% of cases deemed
“idiopathic posterior uveitis
• Initially resistant to conventional therapy with systemic corticosteroids or (IMT),
but favorable response is achieved when patients are switched to systemic
antiviral medication

13. DIAGNOSIS
• The diagnosis of herpetic intraocular inflammation is initially based on the
analysis of clinical features.
• PCR of ocular fluids.
• Other method -intraocular antibody production against different herpes viruses-
ELISA
• Witmer Goldmann Coefficient.
• Diagnostic vitrectomy-(vitreous tap)
• Amount of ocular fluids is a limiting factor to perform diagnostic tests in patients
with a suspicion of viral intraocular inflammation.

14. ARN
• Bilateral disease / systematic involvement-systemic antiviral
• Unilateral –local intravitreal
• Maintanance therapy-continued lifelong / if CD4 >100 /cumm and undetectable viral
load in immunocompromised individual.
• In immunocompetent –mainatinance upto 1-3 months

15. • Intravitreal therapy

16. • Lesions must be stabilized after a mean period of 48 hours.
• In resistant cases, more aggressive antiviral therapy should be initiated based on
intravenous foscarnet or ganciclovir.
• with intravitreal injections of ganciclovir effective in immunocompromised.(ADR
Macular infarction)

17. PROGRESSIVE OUTER RETINAL NECROSIS
• Aggressive antiviral therapy - intravenous foscarnet or ganciclovir and intravitreal
ganciclovir are the mainstay treatment.
• Corticosteroids must be avoided in the majority of cases
IMMUNE RECOVERY UVEITIS
• Systemic or periocular steroids under clinical control of HIV load and CD4 count

18. NNHR
• High dose steroids and conventional immunosuppressors fail to control ocular
inflammation.
• After viral confirmation, the use of intravenous acyclovir or oral valacyclovir
reduces inflammation and allow discontinuing immunosuppressors.
• However, low-dose oral prednisone is necessary in the majority of cases.
• Alpha interferon may be proposed in severe cases