It is very difficult to reach at a specific diagnosis of the tuberculous optic neuropathy as there are no specific diagnostic criteria available [17]. This is due to the limitations of the available tests and difficulty in obtaining the biopsy of the intraocular tissues [3, 18, 19]. Though the situation has improved over past few years with the availability of the polymerase chain reaction for ocular fluid analysis, the limitations relate to the low sensitivity and specificity of this test [20–23]. Gupta et al. [24] established a set of recommendations for the successful diagnosis of the disease. These can be summarized as follows: consistent clinical signs and positive results of ocular investigations or positive results of systemic investigations or therapeutic response to antituberculosis treatment [24]. Using this set of criteria, patients can be classified as either “presumed” or “confirmed” cases [24]. These recommendations were later modified to include the interferon-gamma (IFN-γ) release assay [25–27]. Thus, the modified criteria include consistent ocular signs, active or old tuberculous lesion on chest imaging, positive Mantoux reaction or IFN-γ assay , detection of Mycobacterium tuberculosis DNA in ocular fluid samples on polymerase chain reaction (PCR) , positive microscopy or culture of acid-fast bacilli, and/or positive response to antituberculosis treatment [3] (Table 10.2). It is also mandated to exclude other etiologies for optic neuropathy by necessary investigations including the imaging studies for the optic nerve and brain.

Previously, different treatment regimens have been discussed for the management of ocular tuberculosis [24, 28, 29]. A systematic review and meta-analysis recommended a four-drug regimen including isoniazid, rifampicin, pyrazinamide, and ethambutol for the treatment of intraocular tuberculosis for a total duration of 6–9 months [30]. Previously, the role of corticosteroids in improving the final visual outcome in tuberculous optic neuropathy was being debated, but no useful role has so far been elicited [3]. It is extremely important to work in unison with an infectious disease physician and develop the antituberculosis schedule in managing such cases for better visual outcomes [3, 18, 24, 31].

Another concern while treating the patients on antitubercular regimen is the medication-induced optic neuropathy especially with the use of isoniazid and ethambutol [32–35]. It usually occurs as a progressive, painless, bilaterally symmetrical visual disturbance with temporal pallor of the disc [36]. The toxicity is duration and dose dependent, and the symptoms may appear after the patient has been on the drug for a substantial duration of time [36]. Since the patients already have a compromised optic nerve status, it is imperative to monitor closely for any further optic nerve dysfunction with the use of these medications by evaluating the color vision, contrast sensitivity, and visual fields. An initial improvement in these parameters followed by deterioration after starting medications increases the likelihood of patient suffering from drug-induced toxicity. These cases usually show the red-green color defects, but other defects might also be seen, and the characteristic visual field defect in such cases is the central or centrocecal scotoma with preservation of the peripheral visual field [36]. Retinal nerve fiber layer thickness analysis using optical coherence tomography and visual evoked responses (VER) might have a role in early diagnosis of drug toxicity [37]. In a previous study done by us, we found out that macular fibers were most sensitive to the toxic insult by the antitubercular drugs which was reflected as the significant loss of the thickness of temporal RNFL [38]. Also, in cases of subclinical toxicity, the latency was found to be delayed on pattern VER test [38].

As a preventive measure, pyridoxine is often combined with isoniazid to reduce the risk of drug-induced peripheral neuropathy. On the other hand, complete cessation of the ethambutol intake is warranted if the toxicity is noted due to this drug.

Lastly, it is extremely important to rule out systemic involvement as a large set of patients presenting with tuberculous optic neuropathy has been found to have systemic manifestations [3, 39].