ENT AND OCULAR TUBERCULOSIS Dr Don Gregory Junior

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.

Ø Mode of infection in Head & Neck Region 1) Direct spread by contaminated sputum from a pulmonary focus 2) Hematogenous 3) Lymphatic Ø Cervical lymph node involvement is the most common form of lymph node TB & also the most frequent H&N manifestation of TB. Ø TB of cervical spine may present as torticollis, stiffness of neck muscles. Ø 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 1/3 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.

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 Ø Unexplained hoarseness of voice(98. 6%) Ø Odynophagia/dysphagia(35. 8%) Ø Referred otalgia(28. 6%) Signs Ø Any laryngeal structure can be involved by TB. MC site include true vocal cord, epiglottis, false vocal cord, aryepiglottic folds, arytenoids, interarytenoid area & subglottis. Ø Edema, hyperemia, nodularity, ulceration, exophytic mass, vocal cord thickening & obliteration of anatomical landmarks can be seen. Ø 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 -3 weeks 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 ü pale granulation tissue in middle ear with dilated vessels in anterior part of tympanic membrane.

ü 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 ü Pars flaccida is usually not involved by TB. ü Facial nerve palsy may occur with or without sequestrum. ü Persistent non healing granulations in a post mastoidectomy patients may be due to TB. ü 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 Ø 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.

Ø In the 2 nd type, bony involvement(osteomyelitis) is seen with a sequestrum & fistula formation. It is more difficult to treat. Ø Sinonasal TB can spread to brain or orbit resulting in brain abscess, epiphora & deterioration of vision. Ø Tb of sphenoid sinus may present with blindness & features of cavernous sinus thrombosis with gradual onset & slow progression. Ø 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 7 th & 8 th cranial nerve.

Impact of HIV Infection • Singh etal (1996) reviewed 146 pts of H&N TB. 8 had laryngeal TB, of which 2 were 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 2 nd line drugs may be required for atypical mycobacteria/drug resistant TB.

Role Of Surgery • DIAGNOSTIC INDICATIONS ü Biopsy of mucosal lesions ü Lymph node biopsy where FNAC is inconclusive • THERAPEUTIC INDICATIONS ü Excision of a sinus/fistula with TB infection which fails to heal with adequate ATT. ü Drainage of neck abscess ü Presence of sequestrum in mastoid region ü Repeated drainage/external drainage of retropharyngeal abscess. ü 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 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 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 ü Its an idiopathic, noninfective, inflammatory vasculitis of the retinal vasculature attributed to HY to tuberculoprotein. ü Its an important cause of visual morbidity in healthy young adults especially in Idia. ü Usually affects males in their 2 nd or 3 rd decade. ü Disease becomes bilateral within a few yrs in 90% cases ü Most pts present with painless, sudden visual loss in one eye due to vitreous hemorrhage.

ü 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. ü The new vessels being extremely fragile bleed into vitreous which may lead to retinal detachment & irreversible visual loss. ü 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. ü HPE shows nonspecific perivascular cuff of lymphocytes. ü Empirical ATT is not recommended presently in Eale’s disease

2) Serpigineous Choroiditis Ø Its an idiopathic disorder Ø Gupta etal(2003) have demonstrated M. tb DNA in ocular fluid of these cases. Ø Usually respond to corticosteroids & immunosuppressive therapy. Ø 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 Ø 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. Ø 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. Ø Use of systemic steroids interfere with TST results. Ø 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. Ø 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 ü 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 Ø Evidence of pulmonary or other systemic pathology consistent with TB occuring concurrently with the ocular disease Ø Response of ocular & systemic disease to ATT Ø Exclusion of other etiological causes like sarcoidosis, tumours, secondary metastases Minor criteria Ø Positive IGRA or TST Ø Positive PCR for M. tb in ocular fluids or biopsy

Treatment 1)ATT ü Treatment of ocular TB is on the same lines as treatment of TB elsewhere in the body. ü The disease is said to respond well to standard antituberculosis treatment and there is no role for topical treatment. ü Under RNTCP, patient with giant TB granulomas in choroid & those with vision threatening disease constitute serious form of extrapulmonary TB. 2)STEROIDS ü As an adjuvant to the standard antituberculosis treatment to reduce inflammation. ü Anterior segment inflammation and phlyctenulosis require topical steroids with cycloplegics.

3) Others ü Conjunctival lesions causing only mild symptoms respond to local astringents. ü Mucopurulent discharge suggests secondary bacterial infection & treated accordingly. ü Conjunctival lesions heal without scarring but corneal phlyctenules leave superficial scars of variable severity. ü 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 25 mg/kg/day, incidence of optic neuritis was 1. 3 -15% whereas it was <2% with doses of <15 mg/kg/day. • Most cases of optic neuropathy develop 6 -8 weeks 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 1520 mg/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 200900 mg/day. symptoms have been reported as early as 10 th day. isoniazid is stopped at 1 st 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 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.