Some clinical photographs in this presentation are courtesy
Dr.Brad Bowling (Kanski's Clinical Ophthalmology, 8thEd.)
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2Learning Objectives
? At the end of the class, students shall be able to
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? Understand the pathophysiology of ocular tuberculosis.? Recognize common manifestations of ocular tuberculosis.
? Understand the principles of managing the disease.
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INTRODUCTION
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? Tuberculosis is a systemic disease of protean manifestations.? It is a chronic infection caused by mycobacterium tuberculosis that is
characterized by formation of necrotizing granuloma
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? Tuberculosis primary involves lung? Secondary ocular TB is a common presenting form
? Incidence of Ocular TB ranges from 1.4 - 5.74%.
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? Ocular tuberculosis is an extra pulmonary form.
? Primary infection of the eyes is rare.
? Secondary ocular tuberculosis is the ocular involvement as a result of
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-haematogenous spread from a distant site-a direct invasion from adjacent areas like skin, sinus or cranial cavity
-as hypersensitivity response to distant infection.
? The disease is usually chronic and insidious with exacerbations &
remissions.
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PATHOPHYSIOLOGY
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? Tuberculosis is caused by Mycobacterium tuberculosis? An obligate aerobic ,slow growing ,nonspore forming ,nonmotile
bacterium
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? Humans are the only natural host? End organs with high oxygen tension (apices of the lungs , kidneys,
bones , meninges , eye ) are typically infected
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? In the eyes , Choroid and Ciliary body are mainly affected6
TRANSMISSION OF INFECTION
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? Primary airborne disease? Spreads person to person : cough or sneezing
? Droplets measuring 1 to 5 micron suspended in air for several hours
can harbour the bacteria
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? Usually 5 to 200 inhaled bacteria : sufficient for infection
? About 90 % of infected patients : asymptomatic
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? Epidemiology :
? Varying rates of prevalence have been reported
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? World : USA ? 0.5%, Italy ? 6.31%, Japan -6.39%? India :
? South India - 0.39%*
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? North India - 9.86%**
*Biswas J, Narain S, Das D, Ganesh SK. Pattern of uveitis in a referral uveitis clinic in India. Int Ophthalmol 1996-97;20:223-228
**Singh R, Gupta V, Gupta A. Pattern of uveitis in a referral eye clinic in North India. Indian J Ophthalmol 2004;52:121?125.
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? Pathogenesis :
? Haematogenous seeding
? Primary complex
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? Post primary reactivation of lung lesion ? most common? Bacil i remain dormant for years before they are activated
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9CLINICAL PRESENTATIONS
A) Adnexal manifestations
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B) Anterior segment manifestations
C) Posterior segment manifestations
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D) Neuro ophthalmic manifestationsE) Drug related ocular toxicity
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ADNEXAL MANIFESTATIONS
? 1) Lupus Vulgaris
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? 2) Eyelid Tuberculous Granuloma
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LUPUS VULGARIS? Unilateral , insidious
? Begins as painless , soft , reddish-brown
nodules which slowly enlarge to form
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irregularly shaped red plaque and laterulceration and scarring occur (painful ).
? Often accompanied by lymphadenopathy.
? Complications - squamous cell carcinoma
? Treatment includes ATT.
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EYELID TUBERCULOUS GRANULOMA
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? Unilateral , insidious? Manifests with a violet-brown , non-
tender, mobile nodule.
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? Often accompanied by lymphadenopathy.? The nodule may ulcerate after some time
and spread locally in an irregular fashion.
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? Often accompanied by pain and discharge.? Complications include trichiasis and
entropion.
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13Anterior segment manifestations
? 1) Tuberculous conjunctivitis.
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? 2) Conjunctival granuloma.? 3) Phlyctenular keratoconjunctivitis.
? 4) Tuberculous Scleritis
? 5) Interstitial keratitis
? 6) Iridocyclitis
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TUBERCULOUS CONJUNCTIVITIS
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? 1. Primary ? Unilateral
2. Secondary ? Bilateral
? Mucoid discharge, edema of lids and chemosis
? Large follicles which ulcerate
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? Small, painless, and indolent ulcer,nodule on the tarsal conjunctiva and fornix.
? Preauricular lymphadenopathy.
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CONJUNCTIVAL GRANULOMAS
? A Type IV Hypersensitivity reaction.
? Presents as an inflammatory mass on
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the conjunctiva.? It is usually occurs due to tuberculosis
but can be associated with Staphylococcus
aureus .
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16PHYLYCTENULAR KERATOCONJUNCTIVITIS
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? Manifests as slightly raised, small,pinkish white or yellow nodule
surrounded by dilated vessels
on conjunctiva near the limbus
? Classically, there is no clear zone between
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the limbus and the lesion.? Is a delayed hypersensitivity reaction to
mycobacterial antigens
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INTERSTITIAL KERATITIS
? An inflammation of the corneal stroma
without primary involvement of the
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epithelium or endothelium.? In most cases, the inflammation is
an immune-mediated process triggered
by an appropriate antigen.
? Treatment- systemic antitubercular drugs,
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topical steroids and cycloplegics18
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TUBERCULOUS SCLERITIS? Mostly presents as anterior scleritis
Posterior scleritis is rare .
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? Localized focal elevated nodules
or Necrotizing scleritis.
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? The sclera may be infected by direct spreadfrom a local conjunctival or choroidal lesion or
more commonly by haematogenous spread.
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? This may undergo necrosis and may lead toscleromalacia
? It does not respond to topical steroids and requires
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antituberculous therapy
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ANTERIOR UVEITIS? Acute or Chronic granulomatous
uveitis
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? May be associated with iris or angle
granuloma
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? Mutton fat KPs? Posterior synechiae ?broad based
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? Iris findings
? Nodules at pupillary margin( Koeppe nodule),
? Busacca nodules
? Small gray nodules at iris root ?miliary TB
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? Iris atrophy may be seen in some cases? Severe cases, hypopyon may be seen
? Complications : cataract,glaucoma, vitritis
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INTERMEDIATE UVEITIS
? Low-grade, chronic uveitis
? Vitritis with
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? - snowball opacities? - snow banking,
? - peripheral vascular sheathing,
? - peripheral granuloma.
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22Complications
? Cystoid macular edema
? Cataract
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? Raised intraocular pressure? Peripheral neovascularization
? Retinal detachment
? Vitreous haemorrhage
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23POSTERIOR SEGMENT MANIFESTATIONS
? Choroidal tubercles
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? Choroidal tuberculoma
? Serpiginous like choroiditis
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? Subretinal abscess.24
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Choroidal tubercles? Most common manifestation
of intra-ocular tuberculosis
? Hematogenous spread
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? Less than 5, upto 50 in number? Unilateral or bilateral
? Grayish white to yellow in colour
? Indistinct borders
? Mostly in the posterior pole
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Choroidal tubercles
? Seen in miliary tuberculosis and central
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nervous system tuberculosis
? Active Choroidal tubercles usually
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respond well to ATT and generally takeup to 3 to 4 months to heal.
? On healing,the tubercles result in
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pigmented and atrophic scars.
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CHOROIDAL TUBERCULOMA
? Choroidal tubercle continues to grow,
it forms a solitary mass known as
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tuberculoma.? Present as a solitary, yel owish,
subretinal mass with surrounding
exudative retinal detachment.
? May mimic a choroidal tumour.
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? May be located anywhere? Measures from 4 to 14 mm in size
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CHOROIDAL TUBERCULOMA? May occur in immunocompetent
patients and in patients with
disseminated tuberculosis.
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? On ultrasonography, these lesions aresolid, elevated masses with moderate
to low internal reflectivity.
? Respond well to antituberculosis
treatment.
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SERPIGINOUS LIKE CHOROIDITIS
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? Chronic, progressive and recurrent
inflammation that primarily involves
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the choroid and choriocapillaris.? Progresses to involve the retina
secondarily .
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? These lesions begin in the peri papillary
area and spread centrifugally.
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? On progression, acquires anactive advancing edge
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? It represents an immune-mediated hypersensitivity
reaction with progression despite administration of
antitubercular treatment.
? Antituberculosis treatment in conjunction with oral
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corticosteroids/immunosuppressive agents mayreduce the number of recurrences.
? The healing of such lesions may lead to peripapillary
retinochoroiditis scar.
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30SUB-RETINAL ABSCESSES
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? Results following liquefaction of caseous material in thegranuloma.
? Yellowish lesions associated with overlying vitritis,
retinal haemorrhages and serous retinal detachment.
? Rarely, these lesions can rupture into the vitreous cavity
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and may lead to endophthalmitis or panophthalmitis31
RETINAL VASCULITIS
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? Involves mainly the veins
? Characteristic feature is Periphlebitis
? Associated features
? vitreous infiltrates (vitritis)
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? perivascular cuffing? retinal haemorrhages
? neo- vascularization
? neuro-retinitis
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32NEURO-OPHTHALMIC MANIFESTATIONS
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? The optic neuropathy develops either from direct infection inducedby mycobacteria or from a hypersensitivity to infectious agent.
? The involvement may manifest as
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? papillitis,? retrobulbar neuritis
? neuroretinitis.
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? Clinical features
? Rapid painful loss of vision
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? Vitreous haze? Hyperemia of the disc
? Blurring of disc margins
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? Optic atrophy
? Treatment
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? Systemic steroids: methyl prednisolone 1g IV? ATT
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DRUG-RELATED OCULAR TOXICITY1. Isoniazid
? Optic neuritis
? Steven Johnson syndrome involving lids and conjunctiva
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2. Rifampicin? Orange-red discoloration of tears
3) Rifabutin
? Anterior uveitis .
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354)Ethambutol
Ocular toxic effects include
? Optic neuritis, colour vision abnormalities and visual field defects.
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? Toxicity is dose and duration dependent.? The incidence is up to 6% at a daily dose of 25 mg/kg
and rare with a daily dose not exceeding 15 mg/kg.
? Toxicity typically occurs within 3?6 months of starting treatment.
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36COMPLICATIONS OF OCULAR TUBERCULOSIS
? Cataract
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? Glaucoma? Cystoid Macular oedema
? Retinal detachment
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? Corneal Scarring
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DIAGNOSIS? Confirmation of the diagnosis is a challenge since
intraocular tissue or fluids are examined rarely.
The diagnosis of ocular tuberculosis has remained largely
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presumptive and dependent on associated systemicinfection.
? The diagnosis is typically made based on the clinical
presentation in conjunction with corroborative evidence,
direct evidence, and therapeutic response.
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INVESTIGATIONS
? Corroborative evidence
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? Mantoux test? Chest X RAY / CT Scan
? Serodiagnosis
? Interferon Gamma Release Assays (IGRA )
? Direct evidence
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? Smear and Culture of AFB? PCR
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? Ocular Investigations? Fundus Fluorescein Angiography and ICG
? Optical Coherence Tomography
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? Ultrasonography? Ultrasound Bio Microscopy
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TREATMENT
? Based on evidence - Clinical
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? - Indirect and direct evidence? ATT ? drugs similar to the regimen for pulmonary
TB, with varying duration
? Corticosteroids ? Concomitant use
? Prolonged and difficult in MDR TB
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Treatment
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42Treatment
? Addition of ATT to corticosteroids in uveitis patients
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leads to significant reduction in recurrence.? Systemic corticosteroids used for the first 4?6 weeks,
together with ATT, may limit damage to ocular tissues caused
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from delayed type hypersensitivity.
? One should avoid using corticosteroids alone without
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concomitant ATT.? Close follow-up and monitoring of the liver function and renal
function is mandatory.
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SUMMARY
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? Ocular tuberculosis involves almost all ocular structures except lens.? Commonest manifestation is in the posterior segment.
? Diagnosis depends on clinical findings and suspicion of TB.
? Newer diagnostic modalities, IGRA and PCR are better tools in
diagnosis and for initiating antitubercular treatment.
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? All patients on ATT should be screened for ocular toxicity.44
THANK YOU
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