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Ocular Manifestations in HIV
Infections
Clinically apparent ocular lesions seen in
94% of AIDS patients
Four categories of involvement
Neoplasms (kaposis sarcoma)
Lesions related to microvascular disease
Opportunistic ocular infections
Neuro-ophthalmic abnormalities
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Kaposi sarcoma
AdvancedEarly
Pink, red-violet lesion
Vascular tumour occurring in patients with AIDS
Usually associated with advanced disease
Very sensitive to radiotherapy
May ulcerate and bleed
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Kaposis sarcoma
May be overlooked unless lower lids are
pulled down during exam
Ocular surface or eyelid usually first site fordevelopment of this multifocal neoplasm in
4% cases
Ocular lesion may be the initial or only lesion
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Conjunctiva Dilated vessels at the limbus
Isolated vascular segments of irregular caliber
Sludging of blood flow
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Cotton wool spots Most common retinal manifestation (at
least 2/3 of AIDS cases)
Nerve fiber layer swelling
Stasis of axoplasmic flow
Reflection of retinal ischemia
Spontaneously regresses in 4-6 weeks
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Cytomegalovirus retinitis Early CMV difficult to distinguish from cotton
wool spots
No spontaneous resolution
Relentlessly progressive
Individual foci coalesce and spread outwards
Necrotic retina replaced by thin, glioticmembrane -> retinal detachment
NEED FOR SERIAL EXAMINATION
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Cytomegalovirus retinitis Most common ocular infection (25%)
Full thickness retinal necrosis
Dry, granular, retinal opacification(edema / necrosis)
Hemmorhage and vasculitis
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Cytomegalovirus retinitis Hematogenous spread
Microvasculopathy ->damage vesselwall ->allow access of viral particles to
retinal tissue
Cotton-wool spots precede or occur
concurrently
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Cytomegalovirus retinitis Early lesions adjacent to major vascular
arcades (vascular orientation)
May also occur first in the peripheralretina
Little inflammatory reaction; vitreous
remains clear
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Cytomegalovirus retinitis
Treatment
Ganciclovir (IV or intravitreal at 200
ug/0.1cc); watch out for neutropenia Foscarnet (IV); watch out for kidney damage
(need proper hydration)
AZT (azidothymidine) effective against HIV
but no effect on CMV
Laser - failure to prevent spread of CMV
retinitis
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CONGENITAL
CATARACT
most are bilateral
associated with maternal infection
Rubella, Toxoplasmosis,
Cytomegalic Inclusion Disease
may cause nystagmus
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Lagophthalmos
Insufficient or weak
eyelid closure
May result toexposure keratitis
Treatment: eyelid
taping when
sleeping; artificialtears
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Fungal Keratitis
Rare, but not in P.I.
Farmers
Causative agents: Aspergillus
Fusarium
Candida
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Fungal Keratitis Signs and Symptoms:
Redness, pain, profuse
mucoid discharge ,
intense anterior chamber
reaction(non specific) Slow progression
feathery borders
Satellite lesions
Endothelial plaque
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Fungal Keratitis
Treatment:
Difficult
Drops: Natamycin 5%
Amphotericin B 0.15% eye drops
IV/ Systemic antifungal drugs
If large and with impending perforation
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Fungal Keratitis
Surgery
Therapeutic
transplant
Perforated ulcers
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Acanthamoeba
Protozoa
Contact lens wearers Differentiate from
Pseudomonas (fastprogression, cornealmelt, profuse discharge)
PAIN Radial keratoneurtitis
Disproportionate toclinical signs
Infiltrates Start out as satellite
lesions
Coalesce to form acentral ulceration
ring inflitrates
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Acanthamoeba
Slow progression
Epithelium may be intact
CLUES:Severe pain
Cultures negative for bacterial or fungal
growth
No response to typical antimicrobial or
antifungal therapy
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Acanthamoeba
Treatment: Antiamoebic drugs
Propamidine isothionate
Polyhexamethylene biguanide chlorhexidine
Steroids
controversial
May decrease pain but case delayed healing
NSAIDS: better alternative
Surgery Therapeutic transplants
CONTRAINDICATED in inflamed eyes
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Sample Question
Which therapy is least appropriate for treatment of
dendritic epithelial keratitis due to herpes simplex
virus?
a. Vidarabine ointment 4 times a day
b. Trifluoridine solution 4 times a day
c. Oral acyclovir 2 grams a day
d. Prednisolone acetate 1% qide. Minimal debridement with a dry cotton-tipped applicator
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Viral Keratitis
Herpes Simplex
DNA virus
Common: up to 90% of human population seropositive
HSV1(face, lips, eyes)
Primary infection
In children, usually droplet
subclinical
Recurrence
Immunocompromised state
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Viral Keratitis
Herpes Simplex
Keratitis
Two types Epithelial (HSEK)
Disciform
keratitis
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Viral Keratitis
HSEK Reduced corneal
sensation
Epithelial ulceration Anterior stromal infiltrates
Dendrites
Terminal bulbs
Centrifugal spread toform geographic lesions
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Viral Keratitis
Disciform Keratitis
Reduced corneal
sensation
Epithelial edema
overlying stromal
infiltrates
DM folds
Anterior uveitis
IOP may be elevated
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Viral Keratitis
HSEK Treatment:
Topical Antivirals
Ganciclovir 0.15%
Trifluorothymidine 1%
Toxic
Debridment
Systemic Drugs
Effect disappearswhen drug is removed
For those with 2 ormore attacks/year
Disciform Keratitis Treatment:
Topical Antivirals
Steroids
Given withantivirals
Tapering dose
Small lesions may beobserved
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Viral Keratitis
Herpes Zoster Ophthalmicus(HZO)
Caused by varicella (VZV)
Face lesions (Vesicles)
follow nerve distribution,respects midline
HutchinsonsSign
Keratitis:
Epithelial
Dendrites with nobulbs
NummularSubepithelialopacities
Disciform keratitis
Similar to Herpessimplex
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Viral Keratitis
Herpes Zoster Ophthalmicus:
Other findings
Blepharoconjunctivitis Associated with lid vesicles
Episcleritis
Scleritis
Anterior uveitis Sectoral iris atrophy
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