A high index of suspicion based on the principles mentioned above would help in correctly diagnosing cases of tubercular aetiology . Additional tests which may add value to diagnosis are Mantoux test and Quantiferon TB-Gold test. However due to a high positive rate of these tests in areas endemic for tuberculosis, the specificity of these tests for diagnosing active tubercular infection is low. Importance of contrast-enhanced CT scan of the chest has already been enumerated above.

PCR of aqueous to detect tubercular DNA can also be performed where there is a high degree of suspicion [24].

Standard anti-tubercular therapy (ATT) must be given to patients suspected of having tubercular anterior uveitis. The exact duration of such a therapy is not well defined. However, a minimum of 6 months of therapy must be given, and in some cases the duration may even be extended to 9 months. Additionally topical steroids guided by the anterior chamber reaction and mydriatics/cycloplegics should be given. A careful watch must be kept on the intraocular pressure in such cases.

Choroidal tubercles are the most common presentation of tubercular posterior uveitis [37]. The clinical appearance of choroidal tubercles was first described by Edward Von Jaeger in 1855 [9]. Investigators have demonstrated that they are similar to tubercular granulomas seen elsewhere in the body [38]. Choroidal tubercle-like lesions have also been reproduced in an animal model by injecting guinea pigs with tubercular bacilli [38]. These appear as creamy to yellow coloured, flat to slightly raised deep nodules well under the retinal vasculature. Usually there are less than 5 tubercles in each eye, though multiple miliary choroidal tubercles may be seen which may be up to 50–60 in number [37]. Being deep lesions, their borders may not clinically appear very sharp but are still well defined. They are generally seen in the posterior fundus (Figs. 7.6 and 7.7) [37]. Since most of these lesions do not involve the macula, the patient may not have any ocular symptoms. Even subfoveal tubercles may not present with visual loss if the ellipsoid zone remains intact, and there is absence of subretinal fluid. The best way to visualise these lesions is by a dilated indirect ophthalmoscopic examination of the fundus. The size of these lesions can vary from 1/5th disc diameter to less than one disc diameter in size [37]. These may be bilateral or unilateral. In cases with only choroidal tubercles, the anterior chamber may be quiet with no cells and minimal flare. The vitreous is generally clear. Occasionally, choroidal tubercles may present with granulomatous anterior uveitis with varying degree of vitritis and media haze. Sometimes the detection of these lesions may help in the diagnosis of systemic tuberculosis. Thus in cases of suspected systemic tuberculosis, especially pulmonary, meningeal or disseminated, it is a good idea to get a dilated indirect ophthalmoscopic examination of the fundus done as the presence of these lesions may aid in an early diagnosis of tuberculosis. Illingworth and Wright noted choroidal tubercles in 60% cases (25 of 42 cases) of miliary tuberculosis with or without meningitis [39]. However, only 1 out of 18 patients with meningitis without miliary tuberculosis revealed choroidal tubercles [39]. Choroidal tubercles suggest haematogenous dissemination of tubercle bacillus. In a study on ten proven cases of mycobacterial sepsis from India, six eyes (60%) had ocular involvement of which five cases had choroidal tubercles and one case had retinal vasculitis [40]. After treatment with anti-tubercular therapy, the choroidal tubercles fade, leaving flat hypopigmented patches with variable pigmentation (Fig. 7.8).

Ultrasound B-scan of the fundus may not pick up these lesions as they are not too large and not very thick. Recently optical coherence tomography (OCT) with enhanced depth imaging has been used to better characterise these lesion. On OCT they may appear as well-defined hyporeflective areas in the choroid obscuring the normal choroidal vasculature.

Choroidal tubercles may be associated with overlying subretinal fluid. We have also seen a patient with diabetes and miliary tuberculosis having multiple choroidal tubercles and proliferative diabetic retinopathy with macular oedema (Fig. 7.9). The patient was simultaneously treated with anti-tubercular therapy (ATT) , pan-retinal photocoagulation and anti-VEGF therapy with bevacizumab. This treatment regimen targeted all the pathologies evident in the fundus. We found a good response of this treatment regimen on both the choroidal tubercles and the diabetic retinopathy component (Fig. 7.10). The tubercles usually heal in 3–4 months after ATT [37]. The healing is denoted by decreasing size, depressed scar, well-defined margins and a ring of peripheral pigmentation.

These are larger areas of granulomatous infiltration of the choroid with tubercular bacilli forming a subretinal mass lesion. These may be seen with or without the presence of adjacent choroidal tubercles. These are again best seen using an indirect ophthalmoscope. They appear as large creamy to yellow mounds elevating the retinochoroidal layers (Figs. 7.11 and 7.12). The margins may not be very well defined. There may be associated retinal haemorrhages or retinal folds adjacent to the lesions [37]. They may cause much more inflammation in the eye. Thus patients with these lesions may have associated cells in the anterior chamber with cells in the vitreous. The associated intense inflammation in the choroid can also leads to an exudative retinal detachment (Fig. 7.13). There may also be associated cystoid macular oedema. Sometimes these can also be complicated by formation of secondary choroidal neovascular membranes [41]. Such patients may present to an ophthalmologist with loss of vision due to proximity of these lesions to the macula or optic disc or associated exudative detachment or cystoid macular oedema. If left untreated we have seen these lesions to progress significantly with involvement of adjacent ocular coats. Involvement of sclera may cause pain and presence of fluid in the subtenon space which may be detectable on ultrasound B-scan. Ultimately it may result in panophthalmitis . We have earlier reported one such case of tubercular panophthalmitis [42]. Fluorescein angiography of such lesions reveals an early hypofluorescence in the area of the lesion followed by late hyperfluorescence which may be diffuse or granular in appearance. However fluorescein angiography is not diagnostic of a tuberculoma as other inflammatory choroidal granulomas may also have a similar appearance. Ultrawide field imaging (UWFI) of the fundus might be helpful in detecting granulomas in the periphery and in patients with small pupils. Ultrasound B-scan generally shows a choroidal mound with variable (mild to moderate) internal reflectivity as opposed to a haemangioma which shows very uniform moderate internal reflectivity. Other differential diagnosis may include choroidal metastasis, sarcoid granuloma and amelanotic melanoma. In cases of tuberculomas with internal caseous necrosis and abscess formation, the ultrasound B-scan may reveal an anechoic area within the choroidal mound. Choroidal melanomas typically show an initial high reflective spike followed by low internal reflectivity (high angle kappa) and choroidal excavation.