UVEITIS IN AIDS PATIENTS

1. OCULAR MANIFESTATIONS IN
AIDS
DR SHRUTI LADDHA

2. INTRODUCTION
FOLLOWING HEADINGS :
• Microangiopathy
• Opportunistic infections
• Tumors
• Neuro-ophthalmological alterations

3. MICROANGIOPATHY
• Most common
• cotton-wool spots, retinal hemorrhages and vascular occlusions.
• Generally when CD4<200 /cumm
• Usually these lesions do not cause loss of visual acuity and disappear after 6
weeks.

4. OPPORTUNISTIC INFECTIONS-
CMV RETINITIS
• CMV –most common organism –affect 15 % of HIV positive patients
• CD4<50/cumm
• Minimal vitritis
• Three forms –edematous/fulminant -necrosis and hemorhages
-granular- peripheral ,slowly advances towards post pole
-frosted branch angiitis

5. Edematous/Fulminant Indolent retinitis large posterior retinal tear
with shallow localized
detachment –
there is vascular sheathing
reminiscent of frosted branch
angiitis.

6. TREATMENT
• Bilateral disease / systematic involvement-systemic antiviral
• Unilateral –local intravitreal
• Maintenance therapy-continued lifelong / if CD4 >100 /cumm and undetectable
viral load

7. • Intravitreal therapy

8. IMMUNE RECOVERY UVEITIS
• Following the introduction of HAART, patients with healed CMV retinitis have
displayed conditions of anterior uveitis, vitritis and cystoid macular oedema.
• Due to the patient’s immunological improvement there is a reaction against the
CMV antigens located in the retina, leading to an intraocular inflammatory
process.

9. HERPETIC RETINITIS
Acute retinal
necrosis
Progressive outer
retinal necrosis

10. TOXOPLASMOSIS
• May be bilateral with multiple foci involvement.
• Focal lesion with vitritis
• 50% lesion- associated CNS involvement.
• Oculomotor nerve paralysis, papilledema, optic neuropathies and visual field
defect
• Therefore, cranial CT is indicated in all cases.
• T/T -sulphadiazine, pyrimethamine and folinic acid, but without any systemic
corticosteroids.
• Maintainance treatment continued till CD4 count rises.

11. FUNGAL RETINITIS
• Rare.
• Fungus may reach via hematogenous route
• Most common- Candida albicans , Crytococcus neoformans.
OTHERS
• Paracoccidioides brasilisenses
• Histoplasma capsulatum

12. OCULAR CRYPTOCOCCOSIS
• Mostly secondary to CNS infection.
• Most common –papilloedema –generally without affecting visual acuity.
• Loss of vision- chronic papilloedema, adhesive arachnoiditis, invasion of optic nerve.
• Optic neuropathy,
• optic atrophy,
• oculomotor paralysis
• multifocal choroiditis

13. • C. neoformans can infect all ocular structures including the optic nerve, retinal
vessel, and choroidal stroma, leading, respectively, to papillitis, vasculitis, and
choroiditis in immunocompromised patients.
• Choroiditis- bilateral, multifocal ,no inflammation of anterior segment and
vitreous ,rarely causing vision loss
• lesions are typically yellowish and measure roughly ¼ of the optic disc diameter,
tending to affect the posterior pole, and may or may not be associated to
papilledema
• FFA – Hypo-hyper
• ICGA-hypo throughout.
• T/T-AMB

14. Bilateral multifocal creamy yellow choroidal lesions, mild
optic disc edema, and vascular tortuosity.
OCT- showing a small area of fluid limited by a more
prominent and irregular external limiting membrane.
There is underlying nodular choroidal thickening,
retinal pigment epithelium disorganization and
hyperreflectivity of the overlying photoreceptor later.

15. CANDIDA RETINITIS
• I v drug abusers
• Present like retinitis or endopthalmitis.
• The retinitis may progress towards the vitreous body forming
“vitreous pearls”

16. OCT FINDINGS IN ENDOGENOUS CANDIDA
ENDOPHTHALMITIS
According to the retinal layer of lesion invasion and the lesion location, four types of the
OCT manifestations of the retinal lesions were identified, as follows.
• Type 1 are subretinal macular lesions that originate from choroid and penetrate the
neurosensory retina .
• Type 2 lesions are located in the inner retinal layer and protrude into the vitreous,
without intra- or subretinal fluid . They are always located close to the retinal vascular
arcades and are relatively uniform in size, ranging from one-fourth to one disc diameter.
• Type 3 lesions involve the full-thickness retina and protrude into the vitreous . These
lesions always cause macular edema.
• Type 4 lesions are located in the sub-inner limiting membrane (ILM) of the macula, and
break through the ILM into the vitreous . Type 4 lesions exceed 2 disc diameters.

17. TYPE 1
A)Before treatment. The fundus photograph shows a
yellow–white lesion with a small hemorrhage (white
arrow) on the temporal side of the fovea. The OCT image
shows a macular subretinal lesion originating at the
retinal pigment epithelium/choroid layer (yellow arrow)
and penetrating into the neurosensory retina.
B) Two weeks after treatment (intravitreal injection).
Shrinkage of the subretinal lesion is apparent on the OCT
image.
C) Five months after treatment. The OCT image shows
hyperreflective fibrosis in the subretinal lesion. The inner
choroid is also hyperreflective

18. TYPE 2
a)Before treatment. The fundus photograph shows a
white round lesion (approximately one-half disc
diameter) near the infratemporal vascular arcade
(white arrow). The OCT image shows a lesion in the
inner retinal layer, invading the posterior vitreous. No
intra- or subretinal fluid is present.
b One month after treatment (intravitreal injection).
The OCT image shows shrinkage of the retinal lesion.
c Three months after treatment. In the OCT image,
regression of the retinal lesion and formation of
epiretinal membrane are apparent

19. TYPE 3
Before treatment. The fundus photograph shows a white
fluffy lesion at the posterior pole. The OCT image shows
a highly reflective lesion (yellow asterisk) involving the
full-thickness retina and protruding into the vitreous.
Macular edema is present with subretinal fluid. The
hyperreflective dots in the posterior vitreous are
infiltrating inflammatory cells.
b One week after treatment (vitrectomy). The OCT
image shows shrinkage of the retinal lesion, formation of
epiretinal membrane (yellow arrow) and reduction of the
macular edema
c Three months after treatment. The retinal lesion
almost resolves, and OCT shows a residual pre-retinal
membrane (yellow arrow) close to the optic disc

20. TYPE 4
a Before treatment. The fundus photograph
shows a large lesion at the posterior pole. The
OCT image shows detachment of the ILM (yellow
arrow) and the sub-ILM lesion breaking through
the ILM into the vitreous.
b Two weeks after treatment (vitrectomy). In the
OCT image, the retinal lesion is no longer
apparent, but the nasal retinal edema remains.
c Three months after treatment. The OCT image
shows reduction of the retinal edema and
improvement of the macular foveal structure

21. SYPHILIS
• 0.6% of HIV patients
• Main manifestation- anterior uveitis
• superficial retinal precipitates, exudative retinal detachment, acute syphilitic placoid posterior
chorioretinopathy, papillitis, vasculitis, neuroretinitis, chorioretinitis, and
retinitis(focal/multifocal/punctate/confluent), disc edema
• Ophthalmic syphilis considered to be a part of neurosyphilis and treated accordingly.
Syphilitic retinitis—oedematous disc associated
with retinitis, vaculitis and haemorrhages

22. OD color fundus photograph-Multiple white infiltrates apparently
located at the retinal surface can be seen, resting on an area of the
retina with a “ground glass” appearance at the superior nasal periphery.
b) SD-OCT at the level of the “ground glass” retina. Hyperreflective dots
infiltrating the retina were observed, precluding the individualization of
the layers, with the exception of the RPE.
c) SD-OCT at the level of the apparently superficial retinal white dots.
Focal areas of dense hyperreflectivity within the retina were observed.
d) SD-OCT at the level of the fovea. A serous foveal detachment can be
appreciated. Image quality is poor due to vitreous haze.
PUNCTATE SYPHILITIC RETINITIS

23. PUNCTATE SYPHILITIC RETINITIS(AFTER ANTIBIOTIC
TREATMENT)
e)presence of multifocal areas of RPE atrophy at the
superior nasal periphery.
f) SD-OCT at the level of the focal depigmented lesions-
the inner retina layers' atrophy and focal disruption of
the RPE layer. The underlying choroid seems to be
unaffected.
g) SD-OCT at the level of the fovea- resolution of the
foveal serous detachment.

24. TUBERCULOSIS
• Ocular TB rare in HIV + patients
• Solitary or multifocal choroiditis.
• Lesions are yellowish-white and measure roughly 100 to 200 μ
• No intraocular inflammation
• Diagnosis can be presumed based on the presence of compatible lesions in patients
with diagnosed miliary tuberculosis and/or therapeutic response.
• Sometimes ,infection by MAC

25. Small solitary yellowish choroidal lesion compatible
with presumed tuberculosis choroiditis in a patient
with disseminated tuberculosis and HIV
yellowish subretinal lesion in the superior arcade in a
patient with Mycobacterium avium infection—
presumed Mycobacterium avium choroiditis

26. Pneumocystis carinii (Pneumocystis jirovecii)
• Rare
• Unifocal /multifocal
• Yellowish lesion
• No intraocular inflammation
• Rarely cause vision loss
• Study shown to be seen in those patient
of pneumocystis infection who are
treated with aerosolised
Pentamidine(as it would treat only lung
infection and not systemic infection.
Unifocal choroiditis in an HIV positive patient with
Pneumocystis carinii infection treated with aerosilated
pentamidine—Pneumocystis unifocal choroiditis

27. Bartonella henselae
• Immunocompetent- cutaneous angiomatosis(cat scratch disease) ,neuroretinitis
• Immunocompromised- poorly demarcated -vasoproliferative disease –
conjunctival and peripapillary angimatosis and no neuroretinitis
• T/T antibiotics for 4-6 months, treatment suspension can lead to relapse

28. NEOPLASM
• Kaposis sarcoma- no intraocular manifestation, can affect eyelid and
conjunctiva(looks like subconj h’age)
• NHL- may involve, orbit, conjunctiva, sclera, choroid and retina.
• Squamous cell carcinoma of conjunctiva may occur
SCC of the conjunctiva
Kaposi’s sarcoma of bulbar conjunctiva
presenting as a painless red mass
Kaposi’s sarcoma masquerading as a chalazion and a
subconjunctival haemorrhage in the right upper
eyelid and the left bulbar conjunctiva respectively

29. NEURO-OPHTHALMIC MANIFESTATIONS
• papilledema, optic neuritis, oculomotor paralysis and visual field defects.
• MC – Cryptococcus neoformans
• Any agent which causes an intracerebral mass can lead to neuro-ophthalmological
alterations and this is the case of toxoplasma gondii
• Other agent which can affect optic Nerve-Cryptococcus, CMV, HSV, HZV,Treponema
,rarely Mycobacterium tuberculi