Ocular manifestation of hiv

OCULAR MANIFESTATIONS OF

HIV INFECTION

DR MD SHAHID MANZOORAMUIO, ALIGARH

INTRODUCTION Human immunodeficiency virus infection / acquired

immunodeficiency syndrome (HIV/AIDS) is

a disease of the human immune system caused by

infection with human immunodeficiency

virus (HIV).

leads to gradual decrease in CD4+ T lymphocytes

causing subsequent opportunistic infections and

neoplasia.

70-75% of patients infected with HIV will develop

some form of ocular involvement.

Ocular manifestations of HIV/AIDS

Direct infection by HIV,

Opportunistic infections

Neoplasia and

Drug related

OCULAR MANIFESTATIONS CORRELATING WITH IMMUNE

STATUS AND STAGE OF HIV INFECTION

A ) ADNEXAL MANIFESTATIONS

B) ANTERIOR SEGMENT MANIFESTATION

C) POSTERIOR SEGMENT MANIFESTATIONS

D) NEURO-OPHTHALMIC MANIFESTATIONS

E) ORBITAL MANIFESTATIONS

F) DRUG-RELATED OCULAR TOXICITY IN HIV-

INFECTED PATIENTS

A) ADNEXAL MANIFESTATIONS

1) Herpes zoster ophthalmicus (HZO)

2) Kaposi sarcoma

3) Molluscum contagiosum

4) Conjunctival microvasculopathy

1) HERPES ZOSTER OPHTHALMICUS

5-15% of HIV patients.

Reactivation of a latent infection by VZV in the

dorsal root of trigeminal nerve .

Manifests with a painful maculo -papulo -vesicular

rash .

Involves the upper lid and does not cross the

midline.

Keratitis, scleritis, uveitis, retinitis, or cns

involvement

Cranial nerve palsies

HERPES ZOSTER OPHTHALMICUS

HERPES ZOSTER OPHTHALMICUS

Intravenous acyclovir 10 mg/kg 3 times per day for

7 days,

followed by oral acyclovir 800 mg to 1 g 5 times per

day for an additional 7 days.

This regimen is most effective when started within

72 hours of onset of the vesicular lesions.

This treatment reduces the frequency of

recurrences.

2) KAPOSI SARCOMA

25% of HIV patients.

Human herpes virus type 8

Mesenchymal-derived vascular neoplasm.

Manifests with a violet-brown , non-tender nodule.

Eyelid and conjunctival Kaposi sarcoma tend to mimic chalazion and localized subconjunctivalhemorrhage, respectively.

It can progress rapidly to other sites such as the gastrointestinal tract and CNS

Complications of ocular Kaposi sarcoma include trichiasis and entropion formation. .

KAPOSI SARCOMA

KAPOSI SARCOMA

KAPOSI SARCOMA

Radiation therapy

Intralesional chemotherapy with

vinblastine, alpha interferon, and liposomal

daunorubicin.

Surgical excision of the tumor.

3) MOLLUSCUM CONTAGIOSUM

20% of HIV patients

It is a highly contagious dermatitis caused by DNA

poxvirus, and it may affect mucous membranes as

well as skin.

Manifests with multiple, small, painless, umbilicated

lesions which produce a waxy discharge when

pressured.

A self-limiting disease with spontaneous resolution

taking months to years.

MOLLUSCUM CONTAGIOSUM



Molluscum contagiosum lesions of the skin can be

treated with

Excision (with or without curettage)

Cryotherapy

Topical agents- phenol and trichloroacetic acid.

4) CONJUNCTIVAL MICROVASCULOPATHY

70 - 80% of HIV patients

Increased plasma viscosity

immune-complex deposition are believed to be

involved and

Direct infection of the conjunctival vascular

endothelium by HIV.

These changes include segmental vascular

dilation and narrowing, microaneurysm

formation, and appearance of comma-shaped

vascular fragments.

CONJUNCTIVAL MICROVASCULOPATHY

B) ANTERIOR SEGMENT MANIFESTATIONS

More than 50% of HIV-positive patients

Common symptoms include irritation, pain,

photophobia, redness and decreased vision

1)Keratoconjunctivitis sicca

2) Keratitis

3) Iridocyclitis

1) KERATOCONJUNCTIVITIS SICCA

10-20% of patients who are HIV positive.

The etiology is related to HIV-mediated

inflammation and damage of the accessory and

major lacrimal glands.

Patients complain of burning uncomfortable red

eyes.

Artificial tears and

lubricating ointment.

KERATOCONJUNCTIVITIS SICCA

2) INFECTIOUS KERATITIS

Main etiology –

Viral (VZV and HSV )- most frequent but less

severe

Bacterial and

less frequent but more severe.

Fungal keratitis

The most common fungal organism is Candida,

especially in intravenous drug users and Fusarium

and Aspergillus species .

VZV HSV

Dermatomal

distribution

Complete Incomplete

Pain Increased less

Scarring of skin Frequent Rare

Postherpetic neuralgia Frequent Rare

Dendrites Small without central

ulceration or terminal

bulbs

Large with central

ulceration and

terminal bulbs

Iris atrophy Sectoral Patchy, with no

sectoral

Recurrent lytic

epithelial keratitis

No recurrent Frequent recurrent

VARICELLA-ZOSTER VIRUS KERATITIS

Recommended treatment is

Oral acyclovir 800 mg 5 times per day or famciclovir

125-500 mg 3-5 times per day.

Chronic treatment may be required for VZV

keratitis. This usually minimizes symptoms and

shortens the duration of viral shedding.

Severe disciform stromal keratitis - treated with

topical corticosteroids.

HERPES SIMPLEX VIRUS KERATITIS

Debridement of HSV epithelial keratitis with a dry cotton-

tipped applicator or a cellulose sponge can hasten

resolution and decrease the load of infectious virus and

viral antigens.

Medical treatment includes acyclovir topical 3%

ointment 5 times daily for 14 days or oral dosage form

400 mg 5 times daily for 7 days; or famciclovir 500 mg

by mouth 3 times daily for 7 days.

HSV neurotrophic keratopathy is a condition that

should be managed with nonpreserved lubricants,

eyelid patching, bandage contact lenses, and

sometimes autologous serum and nerve growth factor.

3) IRIDOCYCLITIS

The etiology of iridocyclitis in HIV-positive

patients includes sequelae of retinitis,

retinochoroiditis, and drug toxicity ( rifabutin,

cidofovir), secondary to direct toxic effect upon

the non-pigmented epithelium of the ciliary

body.

Mild iridocyclitis associated with viral retinitis

due to CMV,HSV, VZV.

Severe, seen in association with ocular

toxoplasmosis, tuberculosis, syphilis, or bacterial

or fungal retinitis.

Treatment

Topical corticosteroid drops are used frequently

but with extreme caution and with proper

antimicrobial coverage when infection is

suspected.

If toxicity from the medication is suspected, the

dose should be tapered or the causative agent

should be discontinued.

C) POSTERIOR SEGMENT MANIFESTATIONS

Posterior segment structures involved in HIV-

positive patients include the retina, choroid, and

optic nerve head.

50% of patients who are HIV positive.

Symptoms are floaters, flashing lights, visual field

defect, and decreased visual acuity.

Presence of an afferent pupillary defect strongly

suggests significant retinal or optic nerve

involvement.

Diagnoses often are based on clinical evidence

seen on funduscopic examinations.

POSTERIOR SEGMENT MANIFESTATIONS

1) HIV retinopathy

2) HIV-related retinochoroiditis

1) HIV RETINOPATHY

50-70% of HIV-infected patients

Arteriolar occlusion in HIV retinal

microvasculopathy leads to interruption of the

axoplasmic flow and the subsequent

accumulations of axoplasmic debris, which

manifests as cotton-wool spots.

Increased plasma viscosity, immune-complex

deposition, and a direct cytopathic effect of the

virus on the retinal vascular endothelium are

believed to be involved.

asymptomatic and transient, but it may contribute to

the optic nerve atrophy seen in many of the

patients. Common findings may include the

following:

Cotton-wool spots

Intraretinal hemorrhages

Roth spots (white-centered hemorrhages)

Retinal microaneurysms

No treatment is indicated for HIV retinopathy.

These patients require observation only.

2) HIV-RELATED RETINOCHOROIDITIS

Viruses are the MC

CMV , VZV and, less commonly HSV .

Bacterial causes include Mycobacterium

tuberculosis and Treponema pallidum (syphilis).

Parasitic causes include Toxoplasma gondii and

Pneumocystis jiroveci

Fungal causes include Candida, Cryptococcus

neoformans, and Histoplasma capsulatum, as

well as, Sporothrix, and Aspergillus species.

Cytomegalovirus retinitis

Acute Retinal Necrosis

Progressive Outer Retinal Necrosis

(Varicella-Zoster Retinitis)

Toxoplasma Retinochoroiditis

Tuberculosis.

CYTOMEGALOVIRUS RETINITIS

Most common cause of intraocular infection

Usually in CD4 < 50/microlitre

Painless, progressive loss of vision

It presents with a wide range of clinical

appearances, from cotton wool to confluent areas

of full thickness retinal necrosis.

Infection spreads centrifugally from that focus

with advancement of lesion borders toward the

fovea like “brushfire” pattern at a median rate of

24 μm/day.

The retinitis begins as small, white perivascular retinal

infiltrates .

The classic lesion is a hemorrhagic necrotizing retinitis that

follows the retinal vasculature

Fluffy retinal infiltrates and necrosis are associated with scattered

hemorrhages, this creates what has been called the "scrambled eggs and

ketchup“or ‘pizza pie appearance of severe CMVR

TREATMENT

Oral Valganciclovir.

Oral ,Intravenous, and Intravitreal ganciclovir.

Intravenous and Intravitreal Foscarnet or

combined intravenous Ganciclovir and Foscarnet

Intravenous Cidofovir

Inhibiting CMV DNA polymerase.


Valganciclovir is the drug of choice for the

treatment of CMV retinitis.

Induction is 900 mg twice a day and then 900 mg

once a day for maintenance.

For ganciclovir, start induction with 5 mg/kg IV

every 12 hours for 14 days, then change to a

maintenance IV dose of 5 mg/kg/day for 7 days.

myelosuppression


Foscarnet

Induction with 60 mg/kg IV every 8 hours for 14

days.

Maintenance IV dose of 90-120 mg/kg/day.

Hydration with 1000 mL of isotonic sodium

chloride solution is recommended because of

renal toxicity associated with foscarnet.


Cidofovir

Induction dose - 5 mg/kg IV over 1 hour once

weekly for 2 weeks.

Maintenance dose - 5 mg/kg over 1 hour once

every other week.

Renal toxicity, Iritis and Ocular hypotony.

ACUTE RETINAL NECROSIS

It is a fulminant retinal vaso-occlusive necrotizing

retinitis , usually due to Varicella-Zoster infection,

can also be caused by Herpes Simplex virus or

Cytomegalovirus.

The retina shows small, necrotic yellowish lesions in

the periphery, which rapidly spread into a larger

confluent white area, most often involving the entire

peripheral retina, and then progress toward the

posterior pole.

Optic neuritis and retinal detachment are frequent complications.



Acute retinal necrosis (ARN) frequently is

complicated by anterior uveitis, retinal and

choroidal vasculitis, vitritis, and papillitis.

Episcleritis, scleritis, or optic neuropathy.

are treated with high doses of intravenous

aciclovir or famciclovir, combined with laser

treatment to prevent retinal detachment

PROGRESSIVE OUTER RETINAL NECROSIS

(VARICELLA-ZOSTER RETINITIS)

It is is a rapidly progressive, necrotizing retinitis

caused by Varicella Zoster virus, without vitritis

or retinal vasculitis.

The retina shows typically a white lesion

(multifocal, deep to the retina, opaque, and

patchy) with no haemorrhages or exudates.

Typically, the lesions start from the posterior

pole and spread with extreme rapidity to involve

the entire retina.






Treatment is often unsatisfactory and usually

requires combination of Ganciclovir and Aciclovir.

The prognosis is very poor and retinal

detachment is common.

TUBERCULOSIS

The most common ocular manifestation is

anterior uveitis and disseminated choroiditis.

Manifests as areas of necrosis surrounded by

mononuclear and giant cells.

unifocal or multifocal yellowish, grayish, or

whitish choroiditis, mostly in the posterior pole.

Patients should be given isoniazid (INH) 300 mg

orally daily, rifampin 600 mg orally daily, and

pyrazinamide 25-35 mg/kg orally daily for 2 months;

then, continue with INH and rifampin for an

additional 7 months.

Drug resistance is most common with streptomycin

and INH; however, this may be minimized by the

use of multiple bactericidal antituberculous drugs.

Pyridoxine 25 mg orally daily usually is added to the

regimen to prevent peripheral neuritis.

TOXOPLASMA RETINOCHOROIDITIS

The usual ocular lesion of toxoplasmosis is a

focal necrotizing retinitis, with white infiltration

and surrounding retinal edema.

Unlike in immunocompetent patients, HIV

infected patients often have bilateral and

multifocal disease associated with anterior

uveitis and vitritis with no pigmented scars

adjacent to the areas of retinal necrosis.

Toxoplasmosis in immunocompromised patients

is not self-limiting as it is in imunocompetent

patients.


Immunocompetent Immunocompromised


For active retinochoroiditis within 2-3 mm of the

disc or fovea, which threatens vision, or peripheral

lesion associated with severe vitritis, start first-line

therapy for 3-6 weeks, as follows:

(1) pyrimethamine 75 mg PO load,25 mg PO twice

daily, plus,

(2) folinic acid 3-5 mg PO twice weekly (to reduce

the adverse effect of bone marrow toxicity of

pyrimethamine), and

(3) sulfadiazine 2 g PO load, then 1 g PO 4 times

daily.

D) NEURO-OPHTHALMOLOGIC

MANIFESTATIONS

10-15% of patients who are infected with HIV

common causes of neuro-ophthalmologic

manifestations include

Meningitis,

Meningeal and Parenchymal Lymphoma,

Neurosyphilis, and

Toxoplasmosis.

Neuro-ophthalmologic manifestations include

Papilledema due to increased intracranial

pressure.

Optic neuritis,

Cranial nerve palsies,

Ocular motility disorders, and

Visual field defects

TREATMENT

Radiation and Chemotherapy for Lymphoma

Specific antibiotics for Infectious causes

Systemic steroids are indicated in severe cases of

optic neuritis (high dose, short course).

E) ORBITAL MANIFESTATIONS

The most common complications include

Orbital lymphoma,

Orbital cellulitis due to Aspergillus infection and

Orbital Kaposi's sarcoma

Lymphomas are treated with radiation and

chemotherapy, whereas orbital cellulitis is

amenable to systemic antibiotics.

F) OCULAR MANIFESTATION OF HIV

INFECTION IN CHILDREN

Fewer ocular manifestations of HIV infection

and an especially low incidence of CMV retinitis.

The reason for this difference is unknown, but

may relate to an altered immune response to HIV

or a lower prevalence of CMV seropositivity in

children.

HIV-infected children are, however, at increased

risk for neurodevelopmental delay, a condition

often associated with neuro-ophthalmic

complications.

A fetal AIDS-associated embryopathy,

with downward obliquity of the eyes,

prominent palpebral fissures,

hypertelorism, and

blue sclerae, has also been described

G) OCULAR TOXICITY OF ANTIRETROVIRAL

DRUGS

Rifabutin- intraocular inflammation uveitis- 33%

Cidofovir- uveitis and intraocular hypotony - 25- 30%

Didanosine- retinal pigment epithelial abnormalities;

mottling and hypertrophy accompanied by overall

decreased retinal function .

Gancyclovir & Acyclovir- corneal epithelial inclusion

termed corneal lipidosis.

Lastly, long-term Atovaquone can corneal subepithelial

deposits.

These adverse effects are dose related and resolve

following discontinuation of the drug, with the exception

of the abnormal retinal pigment epithelial changes.

THANK YOU

Ocular manifestation of hiv

Health & Medicine

stage of hiv infection

conjunctival kaposi

kaposi sarcoma25

latent infection

anddirect infection

molluscum contagiosum20

form of ocular involvement

vesicular lesions