2. Outline
Introduction
Adnexal manifestations of HIV infection
Anterior segment
Posterior segment
In Children
In Developing countries
Drug related ocular toxicity
3. Objectives
• Know incidence and prevalence of ocular diseases in HIV patients.
• Identify common ocular diseases in HIV patients.
• Know the clinical manifestations of common ocular diseases.
• Reach a diagnosis of common ocular diseases.
• Know the outline of management and workup.
4. Epidemiology
A cross-sectional clinical evaluation of HIV/AIDS patients at
Gondar Hospital University was undertaken between January
and June 2004.
Results: 125 adult patients were enrolled in the Hospital from
January to June 2004. The majority were males (N=69) and
the mean age was 34 (range: 16-80 years). About 90% of the
patients were in clinical stages III & IV determined according
to the WHO clinical staging method and 60% of them had at
least one ocular manifestation.
5. Ocular manifestations related to HIV/AIDS in 125 patients, Gondar University
Hospital, Northwest Ethiopia, 2004
Ocular diagnosis Number of patients (%)
• Retinal Microvaculopathy 30 (24)
• Neuro-ophthalmic disorders 12 (9.6)
• Uveitis 9 (7.2)
• Ophthalmic herpes zoster 7 (5.6)
• Molluscum Contagiosum 6 (4.8)
• Conjunctival carcinoma 5 (4)
• Seborrheic blepharitis 3 (2.4)
• Vernal conjunctivitis 1 (0.8)
• Sub conjucnctival haemorrhage 2 (1.6)
Total 75 (60)
6. Ocular manifestations of HIV/AIDS patients in Ethiopia and Other African
Countries
Manifestation Ethiopia Burundi Malawi
(N=125) (N=154) (N=99)
• Frequency of ocular manifestation 60% 19% 20%
• Retinal Microvasculopthy 24% 16% 17%
• Herpes zonster Ophthalmicus 5.6% 1% NA
• Anterior Uveitis 7.2% 4% 2%
• CMV retinitis <1% 1% 1%
• Neuro-ophthalmic disorders 9.6% NA NA
• Conjunctival carcinoma 4% NA NA
NA: Not Available
8. Retinal Vasculopathy
• Retinal microvasculopathy occurs in more
than 50% of HIV-infected patients.
• The most commonly observed
manifestation is cotton-wool spots as in the
figure , although intraretinal hemorrhages,
micro aneurysms, and, uncommonly, retinal
ischemia also occur.
9. • Hypotheses regarding the pathogenesis of retinal
microvasculopathy is HIV induced increase in plasma viscosity,
HIV-related immune complex deposition, and direct infection of
the conjunctival vascular endothelium by HIV.
• HIV-associated retinal microvasculopathy is typically
asymptomatic, but may play a role in the progressive optic
nerve atrophy, loss of color vision, contrast sensitivity, and visual
field are observed in HIV-infected patients.
10. Opportunistic Infections
Causes of infectious retinitis,
including
Cytomegalovirus (A),
Varicella-zoster virus (B),
Herpes simplex virus (C),
Toxoplasmosis (D) in four
different patients with AIDS.
11. Cytomegalovirus Retinitis
• CMV retinitis affects 30% to 40% of HIV-infected patients.
• CMV retinitis typically occurs at CD4+ T-lymphocyte counts of less than 50
cells/mm3, and almost always at counts less than 100 cells/mm3.
• Affected patients typically report gradual visual field loss or the onset of
floaters**. Clinical examination shows geographic retinal thickening and
opacification.
• Treatment of CMV retinitis is a complicated, rapidly evolving field. Current
FDA-approved treatments for active retinitis include intravenous
Gancyclovir, Foscarnet, and Cidofovir. Any of the same medicines or the
recently approved oral formulation of Gancyclovir can be used for
maintenance therapy.
• Local therapy with intravitreal injection of Gancyclovir, foscarnet, or
Cidofovir, or via implantation of a slow-release Gancyclovir-containing
reservoir, is also possible.
12. Varicella-Zoster Virus Retinitis
• VZV is the second most common cause of necrotizing retinitis in HIV-infected
individuals, affecting approximately 5% of large cohorts with AIDS.
• Like CMV, VZV produces retinal whitening , occasionally accompanied by intraretinal
hemorrhages. However, VZV retinitis is usually distinguished by its rapid progression,
multifocal nature, and initial involvement of deep retinal layers. The risk of retinal
detachment is greater than observed with CMV retinitis.
• Treatment involves the use of intravenous and intravitreal antivirals, typically
combination therapy with acyclovir and foscarnet.
Herpes Simplex Virus Retinitis
• Herpes simplex virus is a rare cause of retinitis in HIV-infected patients. Like VZV
retinitis, onset of symptoms and disease progression is rapid. Clinical appearance
may mimic VZV retinitis.
• Treatment should include prompt use of intravenous and intravitreal antivirals, again
most typically acyclovir and foscarnet.
13. Toxoplasmosis Retinochoroiditis
• Ocular toxoplasmosis affects less than 1% of HIV-infected patients in most
countries. Toxoplasmosis retinochoroiditis in HIV-positive patients is usually
distinguished by the occurrence of a moderate to severe anterior chamber
and vitreous inflammation, a relative lack of retinal hemorrhage, and the
presence of a smooth rather than granular edge.
• Moreover, unlike toxoplasmosis retinochoroiditis in immunocompetent
patients, HIV-infected patients often have multifocal and bilateral disease,
with no evidence of inactive toxoplasmosis scars.
• Testing should include serology for IgG and IgM toxoplasmosis antibodies,
but may be negative in profoundly immunosuppressed patients.
• Treatment consists of pyrimethamine in combination with a sulfonamide or
clindamycin, either alone or in combination. Chronic or repeated therapy is
often necessary.
• Atovaquone has been used successfully in the treatment of toxoplasmosis
retinochoroiditis in an HIV-positive patient, but it is expensive and has yet
to be shown to be superior to more standard combination therapy
14. Bacterial and Fungal Retinitis
• Ocular syphilis is the most common intraocular bacterial
infection in HIV-positive patients, affecting up to 2% of patients.
Patients may present with either an iridocyclitis or a more diffuse
intraocular inflammation, with or without retinal or optic nerve
involvement.
• Laboratory testing should include both (RPR) or (VDRL) test and
[FTA-ABS] or [MHA-TP]) test. Rarely, these test may be negative
in HIV-positive patients despite active intraocular disease.
• Treatment includes intravenous penicillin G, 24 million units/day
for 7 to 10 days. Recurrences can occur even after adequate
treatment.
15. INFECTIOUS CHOROIDITIS
Infectious choroiditis is uncommon in
HIV-infected patients, accounting for less
than 1 %.
Up to one third of cases have
concurrent CMV retinitis.
Fig. 13. Acute (A) and healed (B)
Pneumocystis carinii choroiditis in a
patient with AIDS.
16. Unusual Malignancies
INTRAOCULAR LYMPHOMA
• HIV-infected patients are at increased risk for developing non-Hodgkin's
lymphoma.
• Although uncommon, cases of intraocular lymphoma have been reported in
HIV-infected patients, and are composed primarily of B cells.
• Treatment includes radiation and chemotherapy.
17. ORBITAL & NEURO-OPHTHALMIC
MANIFESTATIONS OF HIV INFECTION
Orbital Neuro-ophthalmic
Orbital lymphoma Papilledema
Orbital cellulitis Optic neuritis
Orbital Kaposi's sarcoma Optic atrophy
Cranial nerve palsies
Ocular Motility disorders
Visual field defects
18. ORBITAL MANIFESTATIONS OF HIV INFECTION
• Orbital complications, most commonly orbital lymphoma or
orbital cellulitis, occur in well under 1% of HIV-infected
patients.
• Treatment of orbital cellulitis includes systemic antibiotics
and, as needed, surgical debridement.
19. NEURO-OPHTHALMIC MANIFESTATIONS OF HIV INFECTION
• Neuro-ophthalmic manifestations occur in 10% to 15% of HIV-infected
patients.
• Most common findings include ONH edema related to either
papilledema or direct optic neuritis; nonspecific optic atrophy; CN
palsies (especially of the 6th nerve); occulomotor abnormalities, such
as nystagmus, gaze palsies, internuclear ophthalmoparesis, and skew
deviation (Strabismus) ; and visual field defects.
• In most instances, evaluation includes MRI, followed by a LP for cell
count, cytology, culture, and Ab and Ag testing.
• Treatment includes radiation and chemotherapy in the case of
lymphoma, and specific antibiotic therapy for identified infectious
causes. There is currently no treatment for HIV encephalopathy or
progressive multifocal leukoencephalopathy.
20. Fig. 14. Optic disc edema with surrounding cotton-
wool spots and intraretinal hemorrhages due to
neurosyphilis (A) and cryptococcal meningitis with
papilledema (B) in two different patients with
AIDS.
21. OCULAR MANIFESTATION OF HIV
INFECTION IN CHILDREN
• Children appear to have 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.
22. OCULAR MANIFESTATION OF HIV
INFECTION IN THE DEVELOPING WORLD
• The majority of HIV-infected persons live in the developing
world, particularly in sub-Saharan Africa and Southeast Asia.
• Studies of the ocular complications of HIV infection in these
parts of the world are only beginning to appear, but suggest
that CMV retinitis is less frequent than observed in
developed countries, and that otherwise rare ocular
opportunistic infections, such as toxoplasmosis and
tuberculosis, affect 2% to 10% of patients with AIDS.
23. DRUG-RELATED OCULAR TOXICITY IN
HIV-INFECTED PATIENTS
• 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 cause vortex keratopathy.
24. Workup
• Detailed history and complete ophthalmologic examination
• Fundoscopic examination (retinal nerve fiber loss in HIV retinopathy)
• Fluorescein stain corneal dendrites with terminal bulbs.
• VDRL for Syphilis.
• India ink for fungal infections.
• PCR, viral culture.
• Gram’s stain; AFB; Giemsa staining.
• Baseline investigations (before starting antiviral drugs)
25. Bibliography
• Duane's Foundations of Ophthalmology.2007;
• UNAIDS, AIDS epidemic update: Special report on HIV/AIDS:
December 2006. Available from:
http://data.unaids.org/pub/Epireport/2006/2006_Epiupdate_
en.pdf. [Last accessed on 2007 Oct 31]
• Article on Ocular Manifestations of HIV/AIDS patients in
Gondar University Hospital, north west Ethiopia
• UNAIDS/WHO. ADIS Epidemic Update; 2004.
• Disease Prevention and Control Department, MOH. AIDS in
Ethiopia: Fifth Report. June 2004
HIV infection vs AIDS????*<200 CD4/mm3;Opportunistic infections; Unusual neoplasms; High Viral titersLatest advances in HIV???A Mississippi baby born with the AIDS virus appears to have been cured after being treated with an aggressive regimen of drugs just after her birth 2½ years ago.This is the second documented case of a patient being cured of infection with the human immune-deficiency virus. The first being, an adult man known as the Berlin patient, was cured as a result of a 2007 bone-marrow transplant.
Research method that involvesobservation of all of a population or a representative subset, at a defined time.
With the exception of retinal ischemia, these findings are transient.All forms of retinal microvasculopathy increase in frequency in more advanced stages of HIV infection.
The role of retinal microvasculopathy in the development of CMV retinitis is controversial, with some investigators finding no relationship and others suggesting that retinal vascular damage may provide increased access to circulating CMV-infected lymphocytes
Any aspect of the fundus may be involved, including the optic nerve head. Intraretinal hemorrhages are often present.Individualized, based on consideration of the location and extent of ocular and systemic disease, understanding of potential drug-related side-effects, and knowledge of viral response to past treatments.**Floaters—deposits of various size, shape, consistency, refractive index and motility within Eyes Vitreous Humor which is normally transparent. They can cast a shadow or refract the light.
Between 30% and 50% of HIV-positive patients with toxoplasmosis retinochoroiditis will have central nervous system involvement. Sulfamethoxazole and trimethoprim. *Bactrim
Rapid plasma reagin;Venereal Diseases Research Laboratory ; a specific treponemal antibody (Fluorescent treponemal antibody absorption) or (Micro-hemagglutination treponemal palladium)Other bacterial and fungal causes of retinitis or endophthalmitis are rare in HIV-infected patients, but have included Staphylococcus aureus, Histoplasma capsulatum, Sporothrix schenckii, Bipolaris hawaiienisis, and Fusarium Neuroretinitis associated with systemic Bartonella henselae infection has also been described in these patients.
%. Organisms have included Pneumocystis carinii, Cryptococcus neoformans, M. avium complex, Mycobacterium tuberculosis, H. capsulatum, Candida, and Aspergillus fumigatus.
Causative organisms have included Aspergillus, Propionibacterium acnes, Pseudomonas aeruginosa, Staphylococcus aureus, Treponema pallidum, Rhizopus arrhizus Toxoplasma gondii, and Pneumocystis carinii.
Virtually any infectious or neoplastic process can produce these changes, but meningeal and parenchymal lymphoma, Cryptococcus infection, neurosyphilis, and toxoplasmosis are most frequent. More diffuse encephalopathies related either to direct HIV effects (HIV encephalopathy) or to secondary infection with the polyomavirus JC (progressive multifocal leukoencephalopathy) may cause similar complications.
Hypertelorism—Abnormally increased distance b/n two organs.
The reasons for such an altered spectrum of ocular disease in developing countries are almost assuredly related both to poorer medical care and consequent patient death at a higher CD4+ T-lymphocyte level, and to a higher rate of endemic exposure to toxoplasmosis and tuberculosis.
These effects all appear to be dose related and, with the exception of retinal pigment epithelial scarring, tend to resolve once the drug is discontinued.
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