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OCULAR MANIFESTATIONS IN AIDS

Done by,,, Ashwini.K Swaathi.B Supraja .K Kanimozhi .A Karpagam .A Bavithra.k

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OCULAR MANIFESTATIONS
Various opportunistic VIRAL, BACTERIAL AND FUNGAL INFECTIONS
UNUSUAL NEOPLASMS
Kaposi sarcoma Lymphomas involving the retina (primary intraocular lymphoma), adnexal structures and orbit

HIV related MICRO ANGIOPATHY of the retina

OTHER MALIGNANCIES
Squamous cell carcinoma of the conjunctiva
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CORRELATION OF CD 4 CELL COUNT AND HIV ASSOCIATED OCULAR DISEASE CD4 count (cells/cu.mm) Disease
1000
<500

Normal
Kaposi sarcoma Lymphoma Tuberculosis

<250

Pneumocystosis Toxoplasmosis Retinal/conj microvasculopathy

<100

K. sicca VZV retinitis CMV retinitis

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ADNEXAL LESIONS

ULCERATIVE BLEPHARITIS 1 %

Gram Stain

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SQUAMOUS CELL CARCINOMA


Common malignancy of conjunctiva Found mostly in africa Workers who work in sunlight and who are exposed to more UV radiation are affected High titres of HUMAN PAPILLOMA VIRUS is associated with this disease

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SQUAMOUS CELL CARCINOMA OF CONJUNCTIVA


Show spindle cells with frequent abnormal mitotic figures

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KAPOSI SARCOMA
Caused by HUMAN HERPES VIRUS 8 Transmission is through sexual or mostly from mother to child. It mostly presents as a purple nodule. Prevalent in Kenya and Nigeria

nearly 20 % of all malignancies

Epidemic variety first noted in renal transplant patients

30% of all patients with AIDS especially males


Very aggressive and disseminates rapidly

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KAPOSI SARCOMA

No case of ocular Kaposis Sarcoma seen in Indian patients - ???? due to less prevalence of Human herpes virus-8)
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CONJUNCTIVAL MASS

3 months after treatment

Started on HAART and ATT


Conjunctival mass Managed by excision and scleral 3/2/2012 patch grafting
Scleral patch graft
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HERPES ZOSTER OPHTHALMICUS


Apparently healthy young people with HZO
Can cause a persistent chronic epithelial keratitis Treatment Systemic and topical acyclovir

Incidence - 1.68% in our series


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MOLLUSCUM CONTAGIOSUM -1.03%


DNA virus of pox family

Small elevation with central umbilication - characteristic


In healthy individuals Few, unilateral and involve eyelids

In AIDS Numerous and bilateral Excision if symptomatic or causes conjunctivitis Surgery and cryotherapy sometimes ineffective
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OTHER ANTERIOR SEGMENT LESIONS


Idiopathic Anterior Uveitis Herpetic Anterior Uveitis

Infectious keratitis
Bacterial keratitis Doesnt predispose But infection more severe Herpes simplex keratitis

Microsporidiasis Solitary granulomatous conjunctivitis


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Cryptococcus
Tuberculosis Mycotic infections
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Conjunctival microvasculopathy

ANTERIOR UVEITIS
Seen in 88 % of HIV patients in zimbave Etiological agents of anterior uveitis is viral infections , syphilis and tuberculosis. Idiopatic forms are associated with decrease in cell mediated immunity

It may occur after HAART treatment also as a part of auto immune disease.

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ANTEROR UVEITIS
COMMON SIGNS ARE

photophobia pain reduced vision redness

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2000; 48: 311-12

HAEMORRHAGIC HYPOPYON A COMPLICATION OF HERPES ZOSTER OPHTHALMICUS 3/2/2012 16

CRYPTOCOCCUS NEOFORMANS
May result in multifocal choroiditis similar to P carinii Choroidal lesions seen sometimes before systemic infection CNS involvement more common
Cryptococcus in India Ink Preparation Of CSF
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HIV AND DR
Hard exudates seen in DR not seen in HIV retinopathy

In HTN retinopathy associated vascular changes can be noted


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Papilladema & Peripapillary haemorrhages

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HIV RETINOPATHY
Most common ocular finding in patients with AIDS Characterised by retinal microvasculopathy Retinal haemorrhages Microaneurysms Multiple cotton wool spots

Roth spots and ischemic


maculopathy 11% in our series
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Retinal microvasculopathy causing ischemic optic neuropathy

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HIV RETINOPATHY
Cotton wool spots
Oriented along the vascular arcades

Represent focal areas of nerve fiber layer ischemia Regress on their own in 6-9 weeks

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HIV RETINOPATHY
CWS, retinal hemorrhages and MA due to
underlying microvasculopathy hematologic abnormalities such as increased leucocyte activation and rigidity Fundus fluorescein angiogram
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HIV RETINOPATHY
Difficult to differentiate from early CMV retinitis
Periodic fundus examinations are required to rule out any change in the lesions

Correlates well with CD4 counts


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INFECTIOUS DISEASES - RETINA AND CHOROID


Manifestations of disseminated disease in AIDS Principles of therapy Initial high dose induction Maintenance life long - Lower dose To reduce incidence of side effects To maximize quality of life Treatment of ocular infection must take into account the systemic nature of infection and Ocular treatment alone may not affect systemic course
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OPPORTUNISTIC OCULAR INFECTIONS


Retinal and choroidal pathogens
Cytomegalovirus Herpes Zoster / Varicella zoster virus Toxoplasma gondii

Mycobacterium tuberculosis
M. avium intracellulare Cryptococcus neoformans Pneumocystis carinii Histoplasma capsulatum Candida Molluscum contagiosum
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Microsporidia and others

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PATTERNS OF POSTERIOR SEGMENT INFECTIONS


Retinitis more common than Choroiditis
Retinitis in inflamed eyes occur in high CD 4 counts ARN, Toxoplasmosis, syphilis, later cryptococcosis CD 4 count is helpful in arriving at an diagnosis Low CD4 counts are seen in CMV retinitis & PORN
Adjunctive investigations like serology and PCR help clinch diagnosis and so specific treatment can be instituted
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CYTO MEGALO VIRUS INFECTION


Shed in body fluids, asymptomatic in healthy individuals
In immunocompromised major cause of morbidity and mortality High incidence of anti CMV antibodies in general population is evidence of widespread exposure to the virus Double stranded DNA virus Herpes viridae family Before HAART systemic CMV occurring in retina, colon, lung etc most common opportunistic infection in AIDS
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Retina commonly presents with clinical manifestations


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CMV RETINITIS
Before HAART CMV retinitis 15-40%

Median elapsed time between diagnosis of AIDS and development of CMV retinitis was about 9 months
Recent data can occur as long as 3-5 years and usually develops < 50 cells Correlates well with decreased CD4+ cell count

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CMV RETINITIS
Characteristic granular Necrotizing hemorrhagic retinitis Tends to spread along one or more of the vascular arcades Cottage cheese with tomato ketchup or Pizza pie appearance
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CMV RETINITIS

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Frosted branch angiitis - Seen in about 6 % patients

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CMV RETINITIS FULMINANT

brushfire spread from the original lesion


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Fulminant vision threatening CMV retinitis


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CMV RETINITIS

Untreated end stage CMV retinitis

Can be associated with papillitis Late stages, optic atrophy - cause of poor vision
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CMV RETINITIS -COMPLICATIONS


Retinal detachment occurs in up to 50% of patients
Can occur when retinitis is active or quiescent

Myopia additional risk factor

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Healed CMV retinitis Complicated by retinal detachment

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RISK FACTORS

Retinal detachments difficult to repair


Extensive retinal necrosis Multiple holes

Anatomical reattachment 90% of these patients

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PROGRESSIVE OUTER RETINAL NECROSIS - PORN

Acute Retinal Necrosis Syndrome

CRACKED MUD APPEARANCE

Visual loss occurs in 70-85% cases Optic atrophy Retinal detachment


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Deep retinal whitening with Perivascular clearing

CRACKED MUD APPEARANCE

PORN
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OCULAR TOXOPLASMOSIS
PRESENTING SIGNS

leukocoria
fundus yellow white, necrotising lesion wit overlying vitritis MRI showing ring enhancing lesion of left thalamus

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OCULAR TOXOPLASMOSIS IN AIDS


Unique features
Size of the lesions are larger Bilateral

Vitreous reaction may be lesser


CNS involvement present-MRI must Responds to standard treatment

Not self limiting as in immunocompetent

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OCULAR TOXOPLASMOSIS IN AIDS

Various combinations of pyrimethamine, sulfadiazine, clindamycin Steroids with caution Anti toxoplasma therapy to be continued life long
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PNEUMOCYSTIS CARINII CHOROIDITIS


May present with choroidal infiltrates Contains the micro organism If disseminated needs extensive investigations CXR ABG analysis LFT Abdominal CT Biopsy
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OCULAR MANIFESTATIONS OF AIDS


Neuro ophthalmic signs of intracranial disease Cranial Nerve Palsies Papilledema

Visual Field Defects


Optic Atrophy (commonest) Pupillary Abnormalities

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AIDS IN CHILDREN
< 15 yr age group : 5.5% of all HIV + Vertical transmission : 58.33% Ocular involvement : 50 % Most common anterior segment inv:

Anterior uveitis : 33%

Most common posterior segment inv: CMV retinitis : 33%

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AIDS
TREATMENT

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HAART
Highly Active Antiretroviral Therapy

Landmark event in the history of HIV Treatment


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TREATMENT APPROACH - HIV POSITIVE PATIENT


Treatment involves:
1. Inhibiting the replication of the virus using

antiretrovirals
2. Treatment of opportunistic infections 3. Psychosocial support

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HAART -3 GROUPS OF ANTI RETRO VIRALS Nucleoside analogues


Zidovudine Didanosine Zalicitabine Stavudine Lamivudine Abacavir Protease inhibitors Amprenavir Indinavir Nelfinavir Ritonavir Saquinavir Lopinavir (in comination with ritonavir

Non nucleoside reverse transcriptase inhibitors Nevirapine Delaviridine Efavirenz

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HAART WHEN ?
Asymptomatic patients

CD4 count is below 350 cells/l or viral load is above 3050,000 copies/ml Symptomatic patients Irrespective of CD4 count or viral load

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HAART - DOES WHAT ?

Inhibits viral replication Preserve immune function Prevents disease progression Reduces the incidence of opportunistic infections Prolongs survival

The combined use of three or more of these agents is referred to as highly active anti retroviral therapy
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ALL THATS FINE BUT WHAT DO I DO ?

Suspect AIDS
CHECK/ASK VISION Try direct/indirect ophthalmoscopy If disc

ok - no immediate life threatening disease


If edema Immediate referral

NON OPHTHALMOLOGIST
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ALL THATS FINE BUT WHAT DO I DO ? IN A PATIENT WITH AIDS

Regular ophthalmic evaluation


Monthly
If CD4 < 100

2-3 months
If CD4 100 300

Advise ophthal evaluation SOS if


Vision drop + Floaters ++, Flashes ++

Rise or drop in CD4 counts


Any change in drug regimen

NON OPHTHALMOLOGIST
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OPHTHALMOLOGIST AND OPTOMETRIST HAVE AN IMPORTANT ROLE TO PLAY AND SAVE MANY PATIENTS
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REFERENCES
OCULAR LESIONS IN AIDS IN INDIA . By DR . JYOTHIRMAY BISWAS http://www.southsudanmedicaljournal.com/assets/ files/Journals/vol_2_iss_2_may_09/Eye%20Compli cations%20of%20Acquired%20Immune%20Deficie ncy%20Syndrome.pdf CLINICAL OPHTHALMOLOGY , by J.J KANSKI

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THANK U

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