Transcript Slide 1

ENT AND OCULAR TUBERCULOSIS
Dr. Don Gregory
Junior Resident
Dept of Chest & TB
Introduction
• TB in the head and neck region usually present with
lymphadenopathy or chronic inflammation that do not
respond to antibacterial therapy.
• In pre-chemotherapeutic era, patients with active TB
often developed laryngeal,otologic,nasal & paranasal
involvement. But with advent of effective ATT,
incidence of ENT TB has reduced significantly.
• Resurgence of TB as a consequence of HIV infection
& AIDS has brought ENT TB into focus once again.
 Mode of infection in Head & Neck Region
1) Direct spread by contaminated sputum from a
pulmonary focus
2) Hematogenous
3) Lymphatic
 Cervical lymph node involvement is the most
common form of lymph node TB & also the most
frequent H&N manifestation of TB.
 TB of cervical spine may present as
torticollis,stiffness of neck muscles.
 Retropharyngeal/paravertebral abscess may present
with dysphagia/dyspnoea/stridor `
TB of Oral Cavity
• Oral cavity is an uncommon site of TB involvement.
The intact mucosa of oral cavity is relatively resistant
to invasion & saliva has inhibitory effect on growth of
mycobacteria.
• Infection is usually through infected sputum coughed
out by a patient with open pulmonary TB.it can also be
through hematogenous route.
• Tongue is the most common site(50%) and lesions are
usually over the tip,borders,dorsum & base of
tongue.It may be
single/multiple,painful/painless.usually well
circumscribed,but can be irregular.
• Lesions sometimes begin as
nodules/fissures/plaques.
• Initial picture resembles malignancy
• Histopathology confirms diagnosis of TB.
• Secondary involvement of draining lymph nodes
may occur
• Majority of patients have pulmonary TB.
• Other sites of involvement include floor of
mouth,soft palate, anterior pillars & uvula
Laryngeal TB
• Classically develops due to direct spread to the larynx
from contaminated sputum.
• Frequent in sputum +ve patients & most commonly
involves posterior glottis due to pooling of infected
sputum when patient is in recumbent position.this
results in localised edema,granuloma or ulcerations.
• Can also spread by lymphohematogenous route.
Recent evidence suggests that laryngeal TB with
edematous,polypoid panlaryngitis occuring by this
route is increasing.
EPIDEMIOLOGY
• In pre-chemotherapeutic era, laryngeal involvement
was considered a grave prognostic sign indicative of
severe disease & was seen in nearly 1/3rd cases with
pulmonary TB.
• In the present era, incidence of laryngeal involvement
in pts of pulmonary TB ranges from 1.5-50%
• In countries of high TB endemicity, almost all patients
of laryngeal TB have radiological evidence of
pulmonary TB & many are sputum smear +ve.
• In low endemic countries, pts with laryngeal TB
seldom have pulmonary TB.
• However, pts with a heavy bacillary load & strongly
+ve sputum specimen may not have laryngeal
involvement.
PATHOLOGY
• Tubercle bacilli induce low grade inflammation with formation of
typical TB granulation tissue which later undergoes coagulation
necrosis and caseation.
• Laryngeal lesions reveal edema,hyperemia,granulomas or
ulceration.
• Vocal cord thickening & palsy can occur.
• Epiglottis may show irregular margins & nibbled appearance.
• M.tb may be found in subepithelial tissue.
• The process of destruction & repair proceed simultaneously.
• Submucosa of epiglottis & aryepiglottic folds are likely to
undergo fibrous infiltration resulting in pseudoedema, also k/a
turban epiglottis.This lesion is not common in present era.
Clinical Features
Symptoms
 Unexplained hoarseness of voice(98.6%)
 Odynophagia/dysphagia(35.8%)
 Referred otalgia(28.6%)
Signs
 Any laryngeal structure can be involved by TB .MC site include
true vocal cord,epiglottis,false vocal cord,aryepiglottic
folds,arytenoids,interarytenoid area & subglottis.
 Edema, hyperemia, nodularity,ulceration, exophytic mass, vocal
cord thickening & obliteration of anatomical landmarks can be
seen.
 Vocal cord paralysis,subglottic edema/granulation tissue can
cause stridor.
• Laryngeal TB and carcinoma can coexist. C/F may
overlap & lesions may look similar.
• Incidence is reported to be 1.4%
• ATT shouldbe given for atleast 2-3weeks before
initiating treatment of laryngeal carcinoma.
• When TB develops after antineoplastic therapy, the
infection is more severe with a high mortality.
TB Of Salivary Glands
• TB sialitis is usually secondary to TB of oral cavity or
pulmonary TB. Primary TB of salivary glands is rare.
• Parotid gland is most commonly involved.
• C/F may be acute or chronic.
• Acute features resemble acute non TB sialitis &
differentiation may be difficult.
• Occasionally TB may be found following surgery
performed for a salivary gland tumour.
• CXR & FNAC are useful in confirming diagnosis.
TB of Pharynx
• At present, Tonsils & pharynx are uncommonly
involved by TB.
• Presenting features include a)ulcer on the tonsil or
oropharyngeal wall b)granuloma of the nasopharynx
c)neck abscess.
• Co existence of TB & cancer of pharync could be
a)mere coincidence b)metastatic carcinoma
developing in a recent/old TB lesion c)TB infection
engrafted on cancer in full evolution & d)chronic
progressive TB in which cancer develops.
• Lymphoreticular malignancy may be associated with
TB abscess & sinus of the neck.
• Rarely, TB & cancer may involve 2 different organs.
TB of the Ear
• Primary infection of ear is rare.
• TB of external ear is uncommon.However lupus
vulgaris of external ear has been reported.
• Middle Ear can get infected with M.tb by the bacilli
invading the eustachian tube while the infant is being
fed or by hematogenous spread to mastoid process.
• Symptoms include painless otorrhea & hearing loss.
However pts with TB mastoiditis may have otalgia.
• Signs
 pale granulation tissue in middle ear with dilated
vessels in anterior part of tympanic membrane.
 Multiple perforation in tympanic membrane may
occur due to caseation necrosis which later coalesce
to form a large perforation which may involve annulus
as well
 Pars flaccida is usually not involved by TB.
 Facial nerve palsy may occur with or without
sequestrum.
 Persistent non healing granulations in a post
mastoidectomy patients may be due to TB.
 Preauricular lymphadenopathy with postauricular
fistula is pathognomonic of TB otitis media.
TB of Nasopharynx
• TB of nasopharynx is uncommon.
• Most common complaint is nasal obstruction & rhinorrhea.
• Young females in the age range of 20 to 40 yrs are most
commonly involved.
• Most common clinical manifestation include cervical
lymphedenopathy(53%) f/b hearing
loss(12%),tinnitus,otalgia,nasal obstruction and PND(6%
each).adenoid hypertrophy may be seen.
• Systemic symptoms like fever,night sweats,wt loss may be
seen(12%).
• Direct endoscopic examination shows nasopharyngeal
mucosal irregularity or mass in the nasopharynx.
TB of Paranasal Sinuses
• Its nearly always secondary to pulmonary or
extrapulmonary TB.
• Though any sinus may be involved, maxillary &
ethmoid sinus are most commonly involved.
• Infection reaches sinus either by hematogenous
route or by direct extension from TB of skull base.
• Can occur in 2 forms
In the 1st form(sinonasal TB), infection is limited to
submucosa only. Mucosa may be thickened or filled
with a polyp which has a pale & boggy appearance
with minimal purulent discharge.This form is more
common.
In the 2nd type, bony involvement(osteomyelitis) is
seen with a sequestrum & fistula formation.It is
more difficult to treat.
Sinonasal TB can spread to brain or orbit resulting in
brain abscess, epiphora & deterioration of vision.
Tb of sphenoid sinus may present with blindness &
features of cavernous sinus thrombosis with gradual
onset & slow progression.
Rarely TB of maxillary sinus may be associated with
carcinoma.
Nasal TB
• TB of nasal cavity usually manifests as nasal
obstruction & catarrh.
• Physical examination may reveal pallor of nasal mucosa
with minute apple jelly nodules that do not blanch with
nasal decongestants.These nodules may coalesce to
form a granular lesion with subsequent perforation of
septal cartilage.
• Other sites which can be involved are inferior
turbinate,septal mucosa & vestibular skin.
• Nasolacrimal duct involvement is rare.
• TB of nose can cause complications like septal
perforation,atrophic rhinitis &scarring of nasal
vestibule.
Differential Diagnosis
• TB of oral cavity: primary syphilis, fungal infection,
chronic traumatic ulcers, squamous cell carcinoma
• TB of larynx: Squamous cell carcinoma, other
granulomatous diseases such as fungal infections,
syphilis, leprosy, Wegener’s granulomatosis &
sarcoidosis.
• TB of nose & paranasal sinuses: other
granulomatous diseases(here lesions are painless).
Diagnosis
• Diagnosis of laryngeal TB involves demonstration of M.tb in
sputum, laryngeal swab by smear, culture methods & HPE of
biopsy material.coexistent pulmonary Tb should be looked
for.
• TB of the ear should be ascertained by tissue biopsy. TB otitis
media is diagnosed by smear & culture of ear discharge/HPE
of affected tissue.
• TB of nose/PNS/nasopharynx is diagnosed by smear & culture
examination of nasal discharge, nasopharyngeal secretions
collected by nasal endoscopy along with HPE of affected
tissue.
• TB of tongue,oral cavity,salivary glands is diagnosed by HPE
&microbiology of biopsy material .
• PCR seems to be useful in the diagnosisof ENT TB but large
scale studiesare needed to confirm its role.
Imaging in ENT TB
• Radiological findings are nonspecific in CT/MRI.
• Diffuse thickening of epiglottis or vocal cords is
seen.
• Deep submucosal infiltration of preepiglottic&
paralaryngeal fat spaces is not seen even when
there was extensive involvement of laryngeal space.
• In TB of ear, sequestrum may be seen.CT of
temporal bone may show destruction of osseous
chain,sclerosis of mastoid cortex,opacification of
middle ear & mastoid air cells.MRI may show
thickened 7th & 8th cranial nerve.
Impact of HIV Infection
• Singh etal (1996) reviewed 146 pts of H&N TB. 8 had laryngeal
TB, of which 2were HIV positive.
• MC symptoms were hoarseness,odynophagia & dyspnoea
along with systemic symptoms. White exophytic lesions
involving any area of larynx were seen.
• In a retrospective study by singh(1998) in 38 pts of H&N TB in
HIV,cervical LAP(89%) was MC, supraclavicular LN being most
commonly involved(53%) .mantoux test was 61% sensitive in
HIV pts but reduced to 14% in AIDS.FNAC was 94% sensitive
for diagnosing TB irrespective of HIV status.Surgical biopsy
was gold std for diagnosing TB but caused chronic draining
fistulas(14%).
• Children usually presented with otorrhea.
• Lot of confounding factors & illnesses delayed diagnosis.
Treatment
• ATT (for 6 months)is the mainstay of treatment.if
response is inadequate or slow,treatment is
prolonged.
• As larynx heals, fibrosis of laryngeal tissue occur
resulting in sequelae:cricoarytenoid joint fixation,
posterior glottic stenosis & anterior glottic web,
subglottic stenosis,vocal cord scarring.
• Occasionally 2nd line drugs may be required for
atypical mycobacteria/drug resistant TB.
Role Of Surgery
• DIAGNOSTIC INDICATIONS
 Biopsy of mucosal lesions
 Lymph node biopsy where FNAC is inconclusive
• THERAPEUTIC INDICATIONS
 Excision of a sinus/fistula with TB infection which fails
to heal with adequate ATT.
 Drainage of neck abscess
 Presence of sequestrum in mastoid region
 Repeated drainage/external drainage of
retropharyngeal abscess.
 Revision of cosmetically bad scars left after TB infection
has healed.
• Repeated aspiration is preferred over open drainage
for cold abscesses. However if reqd, external
drainage is preferred over peroral drainage to avoid
sinus formation & prevent the abscessfrom draining
into oropharynx.
• Debridement of diseased bone/grafting may be
reqd.
• Superior laryngeal nerve block has been advocated
for odynophagia.
ANATOMY OF THE EYE
OCULAR TB
• Uveitis is the most common manifestation of ocular
TB.
• The incidence of TB uveitis has varied from 2-30% .
The large variation is due to different diagnostic
criteria.
• Ocular manifestations of TB are protean. It can affect
all areas of the visual system, the choroid is probably
the most commonly affected intraocular structure.
Choroidal tubercles constitute the most common
intraocular lesion of TB. Choroid is involved in 1% of
pulmonary TB patients.
• Primary TB of eyelid, conjuctival sac, and optic nerve is
rare.
• Ocular TB is uncommon in patients of HIV AIDS.
• PRIMARY OCULAR TB- when TB lesions are confined to
eyes only. No systemic lesions are clinically evident or
eye has been the initial portal of entry. Eg: epithelial
injury of cornea may lead to primary ocular TB.
• SECONDARY OCULAR TB- ocular infection resulting
from contiguous spread from adjacent structures or
haematogenous spread from lung. Intraocular and
orbital TB are considered to represent secondary
infections.
Eyelid Tuberculosis
• Tuberculosis affects the eyelids infrequently.
• Occurs as a result of spread from face(lupus vulgaris),
lymph node or hematogenous route.
• Lesion begins as red papule that becomes indurated
which enlarges to form a soft “apple jelly” nodule or
plaque that ulcerates. The ulcer is chronic and
painless.
• Atrophic scar, ectropion and destruction of lid may
develop. TB tarsal plate may simulate recurrent
chalazion and finally destruction.
• Regional lymphadenopathy seen in majority cases.
Conjunctival Tuberculosis
• Conjunctival TB and lupus vulgaris are manifestions of primary
TB while tuberculids and phylectenulosis are manifestations of
secondary conjunctival TB.
• Primary lesions present as unilateral nodular or ulcerative
conjuctivitis associated with regional lymphadenopathy.
• Children are most commonly affected by primary type and older
people by secondary type.
• It starts insidiously and 3 to 4 weeks later lead to regional
lymphadenopathy. Enlarged preauricular and rarely
submandibular lymph nodes may suppurate resulting in sinus
formation. Thus , conjuctival TB is one of the causes of
parinaud’s oculoglandular syndrome.
• Types- ulcerative, nodular, polypoid, hyperplastic.
• Solitary tuberculoma involving bulbar conjuctiva are
observed in 2-30% of cases and may simulate
trachomatous lesion. It has propensity to involve
bulbar and upper forniceal conjunctiva. Associated
follicles and corneal infilterations may be
present.Nodule may enlarge to form cauliflower like
lesion with central ulceration.Ulcarative form has
propensity to involve inferior cul de sac.
• Hyperplastic variety develops most commonly in the
fornix and rarely on the tarsus. This form is associated
with severe chemosis and lid oedema and may
assume pedunculated appearance like polypoid form
• Conjunctival tuberculids are a manifestaion of
hypersenstivity reaction, appear as small nodules. It is
associated with involvement of other parts also.
• Phylectenulosis can involve lid margin, cornea or
conjunctiva. Most common site is limbal region.it is a
hypersenstivity reaction to tuberculoprotein. It appears
as small nodule with surrounding hyperemia which
gradually ulcerates and heals without scarring. Limbal
phylectenules leaves a characteristic triangular scar
because conjunctival portion heals without scar unlike
corneal portion.
• M.tb has been demonstrated in only one fourth cases
of conjunctival TB.
• Phlyctenular keratoconjunctivitis usually occurs in
malnourised older children, more in girls.
• Symptoms last for 1-2 weeks and consist of
excessive lacrimation, pain, photophobia and
blepharospasm.
• Severity depends on site involved. Recurrence is
common.
• In the West, staphylococcus has replaced M.tb as
leading cause of phlyctenular conjunctivitis.
Corneal tuberculosis
• Manifests as phlyectenulosis, interstitial keratitis, ulceration and
infiltrations.
• Present as intense photophobia, pain ,blepharospasm
• Phlyctens arise from limbus and heal with variable degree of
scarring and vascularization.Marginal , miliary and fascicular
patterns are seen.
• Intestitial keratisis is associated with more intense scarring and
vasularization in deeper layers. Usually unilateral and involves
lower cornea but is rare entity.
• Sclerosing keratitis may occur as sequelae to TB sclera and
appears as peripheral corneal scleralization. On resolution, it
leaves behind a traingular opacity with base towards limbus.
• Corneal ulcerations usually develop from contiguous spread
from conjuctiva or uveal tract. These ulcers are indolent and
refractory to treatment.
Scleral Tuberculosis
• TB of sclera is characterised by scleral & conjunctival
ulceration.
• Focal necrotising anterior scleritis is the MC
presentation.
• Scleritis develops due to direct scleral infection or by
spread from conjunctiva, uveal tract orby
hematogenous route & produces a nodular lesion.
• O/E preauricular/submandibular LAP is seen.
• Peripheral cornea is secondarily affected &
granulomatous uveitis may also develop
• Scleral nodules may undergo caseous necrosis &
ulceration.later perforation can occur.
Nodular scleritis in a patient with miliary TB
TB of Lacrimal System
• Involvement of lacrimal system by TB is unusual.
• Dacryoadenitisusually developd d/t hematogenous
dissemination, occasionally d/t spread from
conjunctival/corneal disease & infrequently d/t
injury.
• Gradually enlarging painless swelling is seen.
• Regional LAP is a prominent manifestation.
• If eyelid is involved, lid edema & pseudoproptosis
are prominent features.abscess formation with a
chronic draining sinus in upper lid can occur.
• If orbit is involved, proptosis & restriction of upward
gaze is evident.
Orbital Tuberculosis
• Abadie in 1881 first described orbital TB
• Orbital TB can occur in various forms, notably
periostitis, tuberculomas & myositis.
• Occurs by hematogenous spread or by extension of
infection from adjacent structures like PNS.
• Usually U/L & typically occur in first 2 decades of
life.
• Periostitis has an insidious onset & presents as a
chronic,painless inflammation, MC on malar bone.
• Over months ,edema & discoloration of overlying
skin progress to cold abscess, fistula formation,
cicatrization & regional lymphadenitis.
Tuberculoma: Firm masses of chronic granulomatous
inflammation can occur anywhere in the orbit. These
lesions can occur at any age.
• They cause gradual painless proptosis and sclerosis
and thus mimic tumors and fungal infections.
• Occasionally, they involve extraocular muscles and
are bilateral in location.
• Tuberculoma may start in maxillary or ethmoid
sinuses, erode into the orbit and form fistula in the
skin. Overt signs of chronic sinusitis accompany.
Epiphora and epistaxis are also common symptoms.
Tuberculosis of Uveal tract
• M.tb can involve 2 principal internal layers of eye:
uveal and retinal layers.
• May present as choroidal tubercles,disseminated
choroiditis, chronic or acute granulomatous
iridocyclitis, pars planitis, ciliary body granuloma or
endophthalmitis.
• It involves choroid more often than iris and ciliary body
• Mean age of presentation is 32 yr, disease is mostly
unilateral, males and females are equally affected.
Choroidal TB
• Choroidal tubercles and tuberculomata(large solitary masses)
are the most common ocular manifestations of TB.
• Most commonly haematogenous dissemination
• Presence is not diagnostic of miliary TB since can be found in
fungal infections, sarcoidosis, syphilis & metastatic deposits in
choroid.
• Rare in TB meningitis
• May be asymptomatic or presents with blurring of vision
• O/E: choroid tubercles may be solitary or multiple and of
varying dimensions
• Most frequently situated in posterior pole
• Appear as Yellowish grey elevated nodules ± inflammation in
viterous in active stage, retina may be detached
• There is no typical diagnostic pattern on fluorescein
angiography.early hypofloroscense followed by late
hyperflorescense may be seen.
• On USG, dome shaped choroidal masses with low to modearte
internal reflectivity is seen. in cases with extensive caseous
necrosis leading to cold abscess,Loculated anechoic area
within mass may be seen
• Anterior segment is not involved usually.
• Retina can be affected either by direct infection or
hypersenstivity reaction.
• Isolated involvement of retina by direct infection is rare.Usually
retina is affected secondarily from adjacent choroidal lesions.
Tuberculosis Iritis & Iridocyclitis
• Gradenigo in 1869 1st reported HPE evidence of TB
of iris in a patient with miliary TB at autopsy
• TB was an important cause of granulomatous
uveitis until 1960’s.
• Mutton fat keratic precipitates, early formationof
dense synechiae & formation of iris nodules of
koeppe/Bussaca were considered to be
characteristic of TB iridocyclitis. Such nodules need
to be distinguished from sarcoid nodules which are
larger and more pink.
TB Endophthalmitis & Panopthalmitis
• Rarely, TB infection may lead to an endogenous
panopthalmitis or endopthalmitis.
• Mostly in debilitated & IC individuals, drug abusers
or children.
• Painless loss of vision despite significant intraocular
inflammation, presence of iris or scleral nodules,
spontaneous perforation of the ocular coats & early
development of neovascularization of anterior
chamber starting from angle & progressing
centrally.
• Pain may develop d/t secondary glaucoma.
• Endopthalmitis may begin as posterior or anterior
diffuse type.
• In the anterior diffuse type, primary involvement is
restricted to anterior chamber & iris. Pt may have
significant exudation, hypopyon with a silent
posterior segment.
• These cases should be treated early to avoid
enucleation.Also, a completework up to rule out
any focus of systemic infection must be carried out.
Anterior segment photograph in a pt with TB
panopthalmitis
Presumed Intraocular TB
• these are ocular conditions that are presumed to be
due to TB,however actual demonstration of tubercle
bacilli is lacking.
1)Eale’s disease
 Its an idiopathic, noninfective, inflammatory vasculitis
of the retinal vasculature attributed to HY to
tuberculoprotein.
 Its an important cause of visual morbidity in healthy
young adults especially in Idia.
 Usually affects males in their 2nd or 3rd decade.
 Disease becomes bilateral within a few yrs in 90% cases
 Most pts present with painless, sudden visual loss in
one eye due to vitreous hemorrhage.
 Eale’s disease is characterised by retinal periphlebitis &
capillary non perfusion that result in hypoxia. This leads to
neovascularization either on retinal surface or on optic
nerve head.
 The new vessels being extremely fragile bleed into
vitreous which may lead to retinal detachment &
irreversible visual loss.
 Eales’s disease is associated with TB because of
increased prevalence of tuberculoprotein HY, presence of
concurrent active or healed pulmonary TB & response to
ATT in some pts. M.tb DNA have been identified using
PCR on vitreous & epiretinal membranes in many pts.
 HPE shows nonspecific perivascular cuff of lymphocytes.
 Empirical ATT is not recommended presently in Eale’s
disease
2) Serpigineous Choroiditis
 Its an idiopathic disorder
 Gupta etal(2003) have demonstrated M.tb DNA in
ocular fluid of these cases.
 Usually respond to corticosteroids &
immunosuppressive therapy.
 Studies are required as to which subset of patients
might have TB etiology.
Ocular TB in HIV Infected Individuals
• Ocular TB is a rare manifestation in HIV pts.
• A recent study in New Delhi found ocular
manifestations in 6 out of 135 cases(4.4%).5 pts
had Choroiditis(U/L in 2, B/L in 3 cases) & one had
optic atrophy.
• Paradoxical worsening of ocular TB lesions in HIV
pts receiving ART has been described.
Pathology in Ocular TB
• Histopathologically phlyctenules show dense
accumulation of lymphocytes, histiocytes & plasma
cells.Neutrophils are seen in acute phase. Giant
cells & eosinophils are notably absent.M.tb is rarely
seen.
• Choroidal tubercles are similar to tubercles found
elsewhere in the body
• Granulomas may be caseating or non
caseating.Giant cells may be seen.
• TB endophthalmitis is characterized by marked
caseation necrosis & exudation.
PHLYCTEN
Diagnosis of Ocular TB
• Only 25% pts give past history of TB & 50% have
normal chest Xray.
• Orbital radiographs may reveal bony erosions.
• Definitive diagnosis is by demonstrating M.tb in
ocular tissues.But obtaining ocular tissue is
associated with significant ocular morbidity.only
easily accessible sites like eyelid, conjunctiva,
lacrimal gland, sclera can be biopsied.
• Tuberculin skin test
 A positive TST in a pt with granulomatous uveitis was
considered a positive evidence of ocular TB.But a positive TST
is only indicative of infection with M.tb & doesn’t reflect
disease activity.
 Rosenbaum & wernik calculated that a pt with uveitis & a
positive TST has only 1% probability of having active TB.
However, recent conversion from previous nonreactor favours
the diagnosis of TB.
 Use of systemic steroids interfere with TST results.
 In TB endemic countries, a positive TST in isolation has to be
cautiously interpreted. A positive TST is considered to be
supporting evidence in pt with clinical picture highly s/o TB.
 Negative TST is more relevant as it rules out TB in
immunocompetent hosts(not always true as there are several
causes of anergy)
• Serological & molecular methods
Utility of serological tests need further evaluation in
well designed studies with large sample size.PCR
appears to be a promising tool to establish
definitive diagnosis of ocular TB.
• A high index of clinical suspicion is key to early
diagnosis. Hence pts with clinically suspicious
lesions should receive empirical standard ATT.
Suggested criteria for diagnosis of intraocular TB in patients presenting
with a compatible clinical picture in whom there is no definite
histopathological/microbiological evidence of TB
Major criteria
 Evidence of pulmonary or other systemic pathology consistent
with TB occuring concurrently with the ocular disease
 Response of ocular & systemic disease to ATT
 Exclusion of other etiological causes like sarcoidosis, tumours,
secondary metastases
Minor criteria
 Positive IGRA or TST
 Positive PCR for M.tb in ocular fluids or biopsy
Treatment
1)ATT
 Treatment of ocular TB is on the same lines as treatment of TB
elsewhere in the body.
 The disease is said to respond well to standard antituberculosis
treatment and there is no role for topical treatment.
 Under RNTCP, patient with giant TB granulomas in choroid &
those with vision threatening disease constitute serious form of
extrapulmonary TB.
2)STEROIDS
 As an adjuvant to the standard antituberculosis treatment to
reduce inflammation.
 Anterior segment inflammation and phlyctenulosis require
topical steroids with cycloplegics.
3) Others
Conjunctival lesions causing only mild symptoms
respond to local astringents.
Mucopurulent discharge suggests secondary
bacterial infection & treated accordingly.
Conjunctival lesions heal without scarring but
corneal phlyctenules leave superficial scars of
variable severity.
Adjuvant therapy with topical antibiotics like
streptomycin,amikacin & isoniazid have also been
tried in TB scleritis with variable results.
ATT Induced Ocular Toxicity
• Ocular toxicity due to ethambutol , isoniazid &
streptomycin have been well documented,of these
ethambutol has the greatest potential to cause ocular
toxicity.
• Ethambutol related ocular toxicity is strongly dose
related.with a dose of 25mg/kg/day,incidence of optic
neuritis was 1.3-15% whereas it was <2% with doses of
<15mg/kg/day.
• Most cases of optic neuropathy develop 6-8weeks after
starting chemotherapy.
• ADR occur less frequently in pts receiving intermittent
regimens as compared to daily regimens.
• 3 types of optic neuritis occur with ethambutol. Axial,
periaxial & mixed type.Both eyes are usually involved &
visual loss may vary from mild to severe. Colour vision
is also variably affected.
• In the axial form, on visual field recording, pericentral
or peripheral scotomas may be evident. Quadrantic
field defects have commonly been found.
• Although mild disc hyperemia & edema have been
reported,in acute phase of ethambutol toxicity, fundus
examination may be normal.
• Peripapillary splinter hemorrhages, macular edema &
focal pigmentary changes are also described.
• Electrophysiological studies including visual evoked
responses are useful in confirming involvement of optic
nerve & retina in pts receiving ethambutol
• Currently as the dose of ethambutol used is 1520mg/kg/day, toxicity is low & reversible. Hence
VER, ERG are not required in all cases.However a
baseline best corrected visual acuity & colour vision
record should be routinely obtained
• Isoniazid caused optic neuritis at a dose of 200900mg/day.symptoms have been reported as early
as 10th day.isoniazid is stopped at 1st sign of ocular
toxicity. Pyridoxine may be beneficial both in
treatment as well as prophylaxis.
• MC ADR of Rifampicin in eye is conjunctivitis. It can
produce orange tears which can stain contact
lenses.
• Rifabutin can cause endopthalmitis like response.
• Clofazimine has been associated with several ocular
side effects : brownish discoloration of conjunctiva,
brown swirls in the cornea & bull’s eye maculopathy
resulting in visual loss due to macular degeneration.