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OPHTHALMIC PATHOLOGY IN AIDS

Clinical diagnosis for ocular diseases in patients with AIDS is most often made by
funduscopic exam. Findings may include a noninfectious microangiopathy, consisting of cotton-
wool spots with or without retinal hemorrhages. This retinopathy occurs in two thirds of AIDS
cases but can also appear less frequently with HIV infection. Opportunistic ocular infections are
frequent with cytomegalovirus (CMV) and infrequent with Toxoplasma gondii, Pneumocystis
jiroveci (carinii), herpesviruses, Cryptococcus, Candida, Histoplasma, and atypical
mycobacteria. Kaposi sarcoma and malignant lymphomas may infrequently involve conjunctiva,
eyelid, or orbital tissue. Neuro-ophthalmic lesions (cranial nerve palsies, optic neuropathy,
papilledema) appear in less than 10% of AIDS cases but frequently accompany cryptococcal
meningitis.[819,820]
Cytomegalovirus is the most common clinical and autopsy ocular finding in patients with
AIDS. CMV may lead to visual loss via multiple pathways. The most common is retinitis,
which occurs in two thirds of CMV infections. Additional CMV associated ocular lesions
include cataracts, retinal detachment, macular edema, and epiretinal membrane. CMV infection
is most likely to occur when the CD4 count is below 100/µL, so patients receiving antiretroviral
therapy are less likely to develop complications. Patients with CMV retinitis typically present
with progressive painless loss of vision that begins in one eye, but involvement may extend to
both eyes if not treated. Other findings noted by patients include floaters, photopsias, visual field
loss, and blurred vision.[417,819,821]
For presumptive clinical definition of AIDS, diagnosis of CMV retinitis is defined
as:[392]

A characteristic appearance on serial ophthalmoscopic examinations (e.g., discrete
patches of retinal whitening with distinct borders, spreading in a centrifugal manner
along the paths of blood vessels, progressing over several months, and frequently
associated with retinal vasculitis, hemorrhage, and necrosis).

On funduscopic examination, CMV retinitis appears as a full thickness retinal infection
that originates peripherally as perivascular, opaque white, granular areas of retinal necrosis with
associated hemorrhages. It advances centrifugally along retinal vessels, and the advancing edge
has a granular appearance due to engorgement of retinal cells with virions. If it is not treated,
CMV retinitis progresses at a median rate of 24 µm per day and produces full thickness retinal
necrosis that may result in rhegmatogenous retinal detachment (RD) within 3 to 6 months of
diagnosis.[820,821]
Therapies may include ganciclovir, valganciclovir, and foscarnet. Cidofovir has a narrow
therapeutic-toxic window and complications of uveitis and decreased intraocular pressure
(hypotony), so is not often used. Relapse of CMV following treatment can occur. Drug
resistance is uncommon. Resolution of active CMV retinitis may leave retinal scarring and
atrophy with retinal pigment epithelial mottling. Loss of vision may result from retinal
destruction, optic nerve involvement, and retinal detachment. Along with antiretroviral therapy,
the ganciclovir implant and use of valganciclovir have led to better control of CMV retinitis and
lower rates of retinitis progression, retinal detachment, and visual loss. However, even among