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Slide 1
ENT AND OCULAR TUBERCULOSIS Dr. Don Gregory Junior Resident
Dept of Chest & TB
Slide 2
Slide 3
Slide 4
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.
Slide 5
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 `
Slide 6
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.
Slide 7
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
Slide 8
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.
Slide 9
EPIDEMIOLOGY In pre-chemotherapeutic era, laryngeal involvement
was considered a grave prognostic sign indicative of severe disease
& was seen in nearly 1/3 rd 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.
Slide 10
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.
Slide 11
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.
Slide 12
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.
Slide 13
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.
Slide 14
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.
Slide 15
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.
Slide 16
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.
Slide 17
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.
Slide 18
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 1 st
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.
Slide 19
In the 2 nd 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.
Slide 20
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.
Slide 21
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, Wegeners
granulomatosis & sarcoidosis. TB of nose & paranasal
sinuses: other granulomatous diseases(here lesions are
painless).
Slide 22
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 µbiology of biopsy material. PCR seems to be useful in
the diagnosisof ENT TB but large scale studiesare needed to confirm
its role.
Slide 23
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 7 th & 8 th cranial nerve.
Slide 24
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.
Slide 25
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 2 nd line drugs may be required for atypical
mycobacteria/drug resistant TB.
Slide 26
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.
Slide 27
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.
Slide 28
ANATOMY OF THE EYE
Slide 29
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.
Slide 30
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.
Slide 31
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.
Slide 32
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 parinauds
oculoglandular syndrome.
Slide 33
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
Slide 34
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.
Slide 35
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.
Slide 36
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.
Slide 37
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.
Slide 38
Nodular scleritis in a patient with miliary TB
Slide 39
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.
Slide 40
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.
Slide 41
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.
Slide 42
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.
Slide 43
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
Slide 44
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.
Slide 45
Tuberculosis Iritis & Iridocyclitis Gradenigo in 1869 1 st
reported HPE evidence of TB of iris in a patient with miliary TB at
autopsy TB was an important cause of granulomatous uveitis until
1960s. 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.
Slide 46
Slide 47
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.
Slide 48
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.
Slide 49
Anterior segment photograph in a pt with TB panopthalmitis
Slide 50
Presumed Intraocular TB these are ocular conditions that are
presumed to be due to TB,however actual demonstration of tubercle
bacilli is lacking. 1)Eales 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 2 nd or 3 rd 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.
Slide 51
Eales 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. Ealess 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 Eales
disease
Slide 52
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.
Slide 53
Slide 54
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.
Slide 55
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.
Slide 56
Slide 57
PHLYCTEN
Slide 58
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.
Slide 59
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 & doesnt
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)
Slide 60
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.
Slide 61
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
Slide 62
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.
Slide 63
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.
Slide 64
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