Myself Dr. Niraj N. Goswami IInd year Resident RIMS Raichur Thanks to Dr. Siddesh Kumar H Sir Professor and HOD RIMS Raichur Thanks to my seniors for guidance..

1. Posterior uveitis
PRESENTER :DR. NIRAJ N. GOSWAMI
MODERATOR :DR. SIDDESH KUMAR H
MBBS MS FICO PEADS
PROFESSOR AND HEAD OF DEPARTMENT
DEPARTMENT OF OPHTHALMOLOGY
RIMS,RAICHUR

2. Uveitis
 Uveitis is an inflammatory process which in strict definition targets the
uveal tissue( iris, ciliary body, choroid) primarily.
 However, clinically, there is always associated inflammation of other
structures such as :
o Retina
o Vitreous
o Sclera
o Cornea

3. CLASSIFICATION

4. Clinical presentation
 This varies according to the location of inflammatory focus.
 Peripheral lesions: Floaters
 Macular lesions : Impaired central vision, metamorphopsia,
scotoma, photopsia, micropsia, macropsia
 Pain, redness and photophobia are absent unless the anterior
chamber is involved.
 In patients, with posterior uveitis with significant pain,
endophthalmitis or posterior scleritis should be considered.

5. Signs
RETINITIS :
 It can be focal, geographical,
multifocal or diffuse
 Active retinal lesions are
characterized by whitish retinal
lesions with ill defined borders( due
to surrounding edema)
 As lesions heal, the borders
become well defined.

7. CHOROIDITIS :
 Can be focal , multifocal and diffuse or
geographical
 Active lesions are seen as round yellow
nodules with ill defined borders
 The lesions are deeper to retinal vessels
and the overlying retina is usually cloudy
and edematous.
 Vitritis is not present usually unless
accompanied with retinal involvement

8. RETINITIS CHOROIDITIS
Color Whitish cloudy Yellow patchy
Borders Indistinct Distinct well defined
Vitritis Present Sparse or nil
Plane Retinal vessels involved Below retinal vessels
Classical cause Toxoplasma Tb,Sarcoid

9. VASCULITIS
 It can be primary or secondary to retinal or
choroidal involvement
 Venous or arterial, although venous is more
common
 Yellowish or greyish perivascular cuffing, which
may or may not be associated with hemorrhage
 Quiescent vasculitis can leave perivascular
scarring

10. Anterior Segment signs:
 Usually uncommon
 Fine KPs may be visible in some
cases

11. Infective Causes

12. Non infective Causes
 Sarcoidosis
 Birdshot Choroidopathy
 Acute posterior multifocal placoid pigment epitheliopathy
 Serpiginous Choroiditis
 Multiple evanescent white dot syndrome
 Acute macular neuroretinopathy
 Lens induced uveitis
 VKH
 Sympathetic Ophthalmitis

13. Differentia
l
Diagnosis
for
Posterior
Uveitis

14. ETIOLOGY LABORATORY INVESTIGATION
Toxoplasmosis ELISA
Toxocariasis ELISA
Tuberculosis PPQU,Quantiferon TB Gold
T-Spot ,CHEST X RAY
Viral (HSV,VZV,CMV) Aqueous/Vitreous tap/biopsy
for PCR
Ocular Histoplasmosis
Syphilis RPR (Rapid plasma
reagin,Troponema pallidum
antibody
Posterior Uveitis

15. Tuberculous Uveitis
 Causative organism: Mycobacterium tuberculosis
 Primary infection in lung which spreads via bloodstream to other
parts of the body.
 HALLMARK : Necrotising granuloma formation
 In eye, TB mostly presents as uveitis (rich blood supply)
 In endemic areas, it affects all age groups and cause severe
disease, whereas in non endemic areas it affects elderly people
who are immunocompromised.

16. Ocular Manifestations
 ANTERIOR : Anterior uveitis with
MUTTON FAT KPs ,Broad posterior
synechiae and Koeppes nodules
 INTERMEDIATE : snowball opacities,
peripheral vascular sheathing

17. Posterior and Panuveitis
1. Choroid Tubercles
 It is the most recognized feature
 Occurs due to hematogenous spread
 Less than 5 in number ,1-2 mm in size
 Active: Whitish yellowish to grey nodule
with ill defined borders in the posterior pole
 Healed : Pigmented and atrophic scar
 Associated with hyperemic disc

18. 2. Choroidal Tuberculoma :
 Whitish subretinal mass which gradually
becomes yellowish
 Choroidal abscess results from
liquefactive necrosis of choroidal
Tuberculoma
 May cause severe vitritis
Blood vessels
above
Tuberculom
a

19. 3.Multifocal Serpiginous Choroiditis :
 Tb endemic countries
 There is central healing with active amoeboid margins along the vessels
 Spread in centrifugal pattern
 Associated with prominent vitritis
 Does not respond to corticosteroid ,only respond to ATT

20. 3. Retinal Vasculitis :
Common in TB endemic regions
2 forms :
Retinal periphlebitis
Occlusive vasculitis : which causes
neovascularization, vitreous hemorrhage and
tractional retinal detachment

21. 5. Vitritis
6. Macular involvement :
Cystoid macular edema
Epiretinal membrane
Disc Involvement:
-Neuroretinitis
-Optic nerve head granuloma
Other manifestations include :
Phlyctenular Conjunctivitis
Conjunctival granuloma
Exudative RD

22. Diagnosis
 Tuberculin skin test
 IGRA(interferon gamma release assay)
 QuantiFERON TB GOLD Test
 Chest radiography / CT THORAX
 PCR of intraocular fluid
 B scan OCT
 FFA,B SCAN
 aqueous/Vitreous tap
 Granulomatous uveitis + positive TST/IGRA + positive CXR : PRESUMED INTRAOCULAR TUBERCULOSIS
 When this is accompanied by microbiological evidence or ocular tissue biopsy evidence of Mtb is
available : CONFIRMED OCULAR TB

25. Pathology

26. Treatment
 Anti TB drug regimen :
HRZE for 2 months + HR for 4 to 7 months
 Systemic Corticosteroids added to limit damage to ocular tissues
 There can be paradoxical worsening after initiation of anti TB
therapy: This is managed by escalating the steroid dosage [0.5-1.0
mg/Kg] while continuing anti TB therapy.

27. Ocular Toxoplasmosis
 Causative organism :-
 Toxoplasma gondii [Toxon-Arc Shaped]
 Main cause of infectious posterior uveitis worldwide (Most common)
 Obligate Intracellular parasite
 Exists in three form (Depends on external conditions
-Tachyzoites
-Bradyzoites(Tissue cysts)
-Oocytes

28. Systemic disease :
Congenital toxoplasmosis (2nd decade): IUD,
hydrocephalus or microcephaly, mental retardation,
intracranial calcifications etc.
Immunocompetent individuals : asymptomatic,
mononucleosis like symptoms (Fever,phyryngitis,cervical
lymphadenopathy)
Immunocompromised individuals :Reactivation of
previously inactive cyst containing scars is life threatening
complications which are mainly neurological toxoplasmic
encephalitis,retinochoroiditis

29. Life cycle

30. Ocular features
1. Reactivation of intraretinal
cysts causing
retinochoroiditis :
 Yellowish exudative lesion
initially involving the inner
retina and later involving full
thickness of retina.
 There is reactive
inflammation of underlying
choroid.
 Healed lesions can cause
RPE hypertrophy causing
Retinochoroidal scars

31. 2. Inflammatory cellular infiltrate of
overlying vitreous:
 Granulomatous precipitates of
posterior hyaloid
 Dense vitreous opacities or
bands.
 Active lesions can induce vitreous
haze causing HEADLIGHT IN FOG
APPEARANCE

32. 3. Vascular changes :
-Venous >Arterial
 Perivascular sheathing of venules
 Perivascular exudates can cause
vascular occlusions causing retinal
edema and hemorrhages
4. Optic nerve head edema
5. Spill over anterior uveitis(Looks like
Granulomatous Uveitis Koeppes and
bussaca

33. 6. Congenital Toxoplasmosis: macular involvement can
cause Wagon wheel scar in macula

34. Diagnosis
 IgG antibodies : detectable in the serum within 1-2 weeks of initial
infection (indicates infection at some point in the past)
 IgM antibodies positivity indicates that infection acquired within the
last one year.
 Congenital toxoplasmosis serology includes IgA and IgM
 Sabin feldman dye test - Gold Standard (Methylene blue dye )
 PCR testing of intraocular fluid
 Imaging : OCT can demonstrate macular edema, Flourescent
Angiography can demonstrate inflammatory activity, Bscan to
exclude exudative retinal detachment.

37. Treatment
Immunocompetent patients with peripheral lesions and no significant
exudation may be observed
ANTIPARASITIC DRUG + CORTICOSTEROID therapy for 5 – 6 weeks
 Antiparasitic drug : Sulfadiazine + Pyrimethamine
 Corticosteroid : 0.5 -1 mg/kg prednisone with tapering dose
Steroid started 24 hours after antiparasitic drug and is tapered off before it
is stopped.
 Intravitreal injection of CLINDAMYCIN + DEXAMETHASONE (single or
repeated injections)

38. In pregnancy, 10-90 rule
1st trimester : Spiramycin +sulfadiazine
2nd trimester : Spiramycin+Sulfadiazine+Pyrimethamine+Folinic
acid
3rd trimester : Spiramycin+Pyrimethamine+Folinic acid
Immunosuppressed individuals and congenital toxoplasmosis are
treated regardless of the presence of retinochoroidal lesion
Standard treatment for newborn :Pyrimethamine +Sulfadiazine
+Folinic acid

39. Cytomegalovirus Retinitis
 Causative organism : cytomegalovirus/HHV5 (Beta Herpesviridae)
 This is usually asymptomatic and manifests only in
immunocompromised individuals
 It is a common opportunistic infection associated with AIDS
(CD4count<50)
 It can affect affect various organs such as LUNGS, CNS, SKIN and
EYES

40. Ocular features
Symptoms include :
 Photopsia
 Loss of vision
 Floaters
 Eye pain(uncommon)
 It can cause anterior uveitis associates with AC cells, flare and
stellate KPs.
 Episodes of elevated eye pressure with active inflammation can be
seen(Posner schlossman syndrome)

41. Posterior segment features
1. Retinitis and Vasculitis
 Initially there is a solitary white lesion with granular borders
 Associated with vasculitis which eventually causes FLAME shaped
hemorrhages (PIZZA PIE appearance)
 Macular involvement causes vision loss
 Initially unilateral, but later progresses to become a bilateral disease
 INDOLENT FORM : peripheral granular opacities with occasional
hemorrhage
 FULMINANT FORM : Vast areas of necrosis with prominent hemorrhages
along with areas of progressive retinal atrophy

43. 2. Frosted Branch angiitis : due to severe
vascular sheathing(arterioles or venules
3. Optic Neuritis
4. Retinal necrosis : When active
inflammation settles down areas with
irregular pigmentation, atrophy and
holes are seen.
This can lead to RRD
5. Immune recovery uveitis : when ART
started the sudden increase in immunity
cause further inflammation (IRIS)

44. Diagnosis and Treatment
Diagnosis is mainly by PCR of ocular fluids(aqueous and vitreous)
Treatment :
 Retropositive patients should be started on HAART
 Systemic and intravitreal antiviral agents
VALGANCICLOVIR is the preferred agent
Induction : 900mg BD x 3 weeks
Maintenance : 900mg daily
Intravitreally : valganciclovir 2mg weekly injection(disease progression or
macula involved)
 Vitrectomy with endolaser demarcation and silicone oil tamponade can be
used incase of retinal detachments
 Steroids are useful in immune recovery uveitis and for frosted branch angiitis

45. Ocular Histoplasmosis
 Causative organism : Histoplasma capsulatum
 It is a dimorphic fungus
OCULAR features :
o Multiple white atrophic chorioretinal spots
o Peripapillary atrophy
o Absent vitritis
o Choroidal neovascularization is a late feature which can cause
accumulation of subretinal fluid and hemorrhage

46. Treatment
These patients are asymptomatic unless they develop choroidal
neovascularization in peripapillary or macular regions
Treatment involves
 Intravitreal anti VEGF injection
 Laser photocoagulation
 Ocular photodynamic therapy with verteporfin

47. References
1. Kanski’s Clinical Ophthalmology 9th
edition
2. Myron Yanoff 5th
edition
3. The Will’s Eye manual 7th
edition
4. AAO retina and vitreous