Ocular Manifestations of HIV Power Point

Ocular Manifestations of HIV
-Reported in 70% of patients with HIV

-It may be the first sign of disseminated systemic infection.
-HIV has been demonstrated in tears, conjunctival

epithelial cells, corneal epithelial cells, aqueous, retinal
vascular endothelial cells,& retina.
-Although transmition of HIV by ophthalmic instruments

for exam has not been reported precaution is
recommended in handling instruments.
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Ocular manifestations of HIV includes
 *Kaposis Sarcoma
 * Molluscum contagiosum
 * Herpus Zoster
 * Squamous cell CA of the conjunctiva
 * HIV microangiopathy of the retina
 * Various opportunistic viral, bacterial, fungal, and
protozoal infections
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KAPOSIS SARCOMA
-Incidence……Before HAART---30% AND after HAART

—20%
-AIDS associated k.s is aggressive and disseminated to
systemic organs like lung, liver, GIT.
-Recent evidence --- originates from HHP8
-Three clinical stages
 * Stage I & II tumors are patchy , flat (<3mm in
height) and less than 4 months in duration.
 * Stage III tumors are nodular elevated, (>3mm In
height) and of > 4 months duration.
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TREATMENT
Depends on the stage of the diseases, location of the
tumor, and presence or absence of disseminated
diseases.
Stage I & II ---Local excision +/- Cryotherapy
Stage III---Radiation or cryotherapy
** Chemotherapy for systemic dissemination
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MOLLUSCUM CONTAGIOSUM
-Caused by Pox virus
- Characteristic lesion on the skin
 *Small elevated with central umblication.
- Lesions in healthy individuals is few and unilateral but
in Aids patients it is multiple and bilateral.
- TREATMENT
 -Is indicated if it is symptomatic or causes
conjunctivitis
 * Treatment is by excision or cryo
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CONJUNCTIVAL SQUAMOUS CELL CA
-Risk factors
 *UV radiation
 * Viral infection
 * Genetics
-C/F
 -It grows in the interpalpebral area
 - Has a broad base
 -Has papiliform growth
 - Usually superficial (Histologic invasion beneath the epithelium
basement membrane is present)
 - Infrequently penetrates the sclera
 -Engorged conjunctival vessels feed the tumor.
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TREATMENT
1.Excision of the tumor
*With 4 mm tumor free margin
*With thin lamellar sclera flap
* Treat the base of the sclera with absolute alcohol and cryo to the
conjuctival margin
2. Exentration
* For extensive external spread
* Intraocular invasion
** Invasion of the iris or trabecular meshwork provides an access to the

systemic circulation.
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Herpes Zoster Ophthalmicus
-occurs from reactivation of VZV infection
-Is self limited in children but sever in elderly or
immunocompromized.
 CLINICAL PRESENTATION
 * Blepharo conjunctivitis/ * Epithelial
keratities/* Stromal keratities
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Diagnosis---- Clinical
Treatment -----with systemic antiviral
 Valacyclovir 1 gm po 3x per day for14 days
 Acyclovir 800mg po 5x per day for 14 days
Treatment of post herpetic neuralgia
* Capsasin cream / * Amitriptyline /*
Carbamazepine
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POSTERIOR SEGMENT INVOLMENT

Visual morbidity in AIDS patients occurs primarily
with posterior segment involvement particularly due
to CMV, T.Gondi, and Herpus Zoster virus,
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CMV RETINITIES
-CMV—is a double stranded DNA virus

-CMV retinitis is the most common ocular
opportunistic infection in AIDS patients.
-Incidence—Prior to HAART 30% in patients with
CD4 count of <5o cells/nl.
- HAART has reduced the incidence of new cases by
80%.
- Transmission… By contact with blood and body
secretion.
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C/F
Early it mimics cotton wool spot and is distinguished
by it’s inevitable progression without treatment.
Late classic retinitis presents with large area of retinal
hemorrhage against a background of white edematous
or necrotic retina.
 Boarder is clearly demarcated and irregular, appearing
in the posterior pole from the disc to the vascular
arcades.
Later may cause Retinal detachment as a complication.
15
16
DIAGNOSIS
In immunocompromised patients is clinical
In atypical cases PCR of the aqueous or vitreous.
TREATMENT
-HAART plus antiviral
-Antiviral drugs
 Gancylovir Intra venous 5mg 2x per day for 2 wks
 Then *Gancylovir Intra venous 5mg 1x per day OR
 *Gancyclovir 3-6 gm po per day untile CMV becomes
stable
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- Response to treatment—80-100%
-Contralateral eye involvement—15%
Alternatives to gancylcovir
Valgancyclovir 900mg po per day for 2 wks then 900mg po per day maintenance
- Valgancyclovir is equally effective like iv gancylcover
-Decreases systemic toxicity related to iv gancyclovir
* Foscarnet
* Fomivirsen
Treatment of relapse
-Re-induction of combination of drugs
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IMMUNE RECOVERY UVEITIS
An anterior or intermediate uveitis with or without
CME that occurs in patients with preexisting CMV
retinitis who improves their immune status with
HAART.
It occurs in 20% of patients with HIV with improved
immune function following HAART.
CD4 at least > 50-100/nl
Treatment is with steroids but Patients with IRS have
macular edema resistant to steroid therapy.
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TOXOPLASMOSIS
The most common cause of posterior segment infection
world wide.
-Caused by T.gondi –an obligate intracellular parasite.
- Asymptomatic in healthy but fulminant in AIDS patients.
TRANSMITION
-Eating or drinking raw meat, milk or contaminated water.
-Transplacental-
 Organ transplantation
- Blood transfusion.
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Congenital toxoplasmosis
 Risk is law if the mother acquires the disease in 1st
trimester (20%) and increases in the 3rd trimester
(59%)
 Most infected fetus are asymptomatic but may
present with
 Hepatoslenomegaly, lymphadenopathy,
retinichoroiditis, hydrocephalus, encephalitis,
intrachranial calcification.
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Acquired toxoplasmosis
Subclinical / Asymptomatic In healthy but fulminant

in AIDS patients.
 Retinochoroiditis may be a sol clinical manifestation.
C/F..Of Toxo in acquired or reactivated cases

-Unilateral blurred vision with floaters
-Mild to moderate granulomatous uveitis
-10-20% of patients have acutely raised IOP
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-Fundus
 Focal white retinitis with overlying moderate vitreous
inflammation<< Head light in the fog>> often adjacent to a
pigmented chorioretinal scar most commonly in the
posterior pole.
 Vessels around the lesion may have sheathing.
** Aids patients may have atypical presentation with bilateral

and multiple lesions with or without scar bilaterally.
**Complications like cataract, glaucoma, CME, CNV, and
Retinal detachment can occur.
23
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DIAGNOSIS
Mainly clinical but serologic tests like
Anti toxo
IgG—appears in the first 2 weeks after infection and remains positive lifelong.
Crosses the placenta
When positive supports the diagnosis
When negative it essentially excludes toxo
IgM—Does’t cross the placenta

When positive confirms congenital toxo
Indicative of acquired toxo in adults
PCR—Detects T.gondi DNA in Aqueous and vitreous

Especially useful in atypical cases
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TREATMENT
-Limits the progression and severity in AIDS patients
- is almost always indicated in immunocompromised patients,
congenital toxo, and pregnant lady with toxo.

*Indication in healthy patients
 1. Lesion threatens the optic nerve and fovea
 2. Reduced visual acuity
 3. Lesion associated with sever vitreous inflammation.
 4. Presence of multiple active lesions
 5. Lesion greater than 1 disc diameter.
 6. Persistent disease greater than one month.
26
- Classic regiemen for treatment of toxo is a triple
therapy
 1. Pyrimetamin 50-100mg/d po for 2 days
 25-50mg/d for 4-6 wks
 2.Sulfadiazin 2-4 gm /d po for 2 days
 0.5-1gm/d for 4-6 wks
 3. Folinic acid 5mg po every other day 4-6 wks
 4. Predenisolon 0.5-1 mg/kg /d depending on the
severity of inflammation for 3-6 wks
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* Steroids can be initiated together with or after 48hrs of antimicrobial
therapy in immunocompitent patients but should be avoided in AIDS
Patients
* Tapper according to the clinical response.
* The use of systemic steroid without antimicrobial cover or the use of

long acting periocular/intraocular steroid drugs are contraindicated
because these agents have been associated with sever uncontrollable
inflammation and loss of the eye.
* Topical steroids can be used liberally in the presence of prominent

anterior segment inflammation.
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* Duration of treatment can be extended more than 6
wks with persistent disease activity.
ALTERNATIVE DRUGS
 Clindamycin/ Co.trimoxazole/ Azitromycin/
Spyramycin/ Atovacone.
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PROGRESIVE OUTER RETINAL NECROSI
Caused by HZV
IS a rapidly progressive necrotizing retinitis that occurs in severely
immunocompromised patients like AIDS with CD4 count of <50/nl
C/F
- Painless reduction of vision in one or both eyes
-No or minimal a/c or vitreous inflammation
-Multifocal peripheral necrotizing retinitis which involves the
entire retinal surface and depth within days
- Retinal detachment can occur as a complication
-Prognosis is poor despite antiviral treatment
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TREATMENT
 -- Gancyclovir plus Foscarnet loading followed by
long term po Gancylovir to prevent recurrence.
 _ don’t use steroids
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THANK YOU
33

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Ocular Manifestations of HIV

-Reported in 70% of patients with HIV

-HIV has been demonstrated in tears, conjunctival

-Although transmition of HIV by ophthalmic instruments

-Incidence……Before HAART---30% AND after HAART

** Invasion of the iris or trabecular meshwork provides an access to the

-CMV—is a double stranded DNA virus

Subclinical / Asymptomatic In healthy but fulminant

C/F..Of Toxo in acquired or reactivated cases

** Aids patients may have atypical presentation with bilateral

IgM—Does’t cross the placenta

PCR—Detects T.gondi DNA in Aqueous and vitreous

* Tapper according to the clinical response.

* The use of systemic steroid without antimicrobial cover or the use of

* Topical steroids can be used liberally in the presence of prominent

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