Bilateral tuberculous neuroretinitis in a young female with disseminated systemic tuberculosis

A 27-year-old female presented with bilateral progressive painless blurring of vision with headache. On examination, her visual acuity (VA) was 6/18, N12 in the right eye (OD) and 6/6, N6 in the left eye (OS). Color vision was defective with sluggishly reacting pupils in both eyes (OU). Visual fields showed central scotoma in OU [Figure 1]. Fundus showed optic disc edema and incomplete macular fan hard exudates in OU suggestive of neuroretinitis [Figure 2]. Past systemic history was uneventful. Blood pressure was normal. Systemic investigations revealed a positive Mantoux test (>10 mm) and a positive interferon gamma release assay for tuberculosis (TB). High-resolution computed tomography of the thorax revealed centrilobular emphysema with enlarged hilar lymph nodes [Figure 3b and c]. Magnetic resonance imaging of the brain showed multiple tuberculomas in the left frontoparietal lobe [Figure 3a]. A uveitic work up was done to rule out other common causes of neuroretinitis like syphilis and cat scratch disease and was found to be negative. Optical coherence tomography of macula OU showed attached fovea with peripapillary elevation [Figure 4]. Investigations to rule out immunosuppression including serology for human immunodeficiency virus were negative. She was referred to pulmonologist for disseminated TB and was started on antituberculous treatment (ATT) – isoniazid, rifampicin, amikacin, and pyrazinamide for 18 months. In view of optic nerve involvement, ethambutol was avoided. The patient was also started on oral prednisolone in tapering doses after 2 weeks of ATT. At the completion of ATT, her VA was 6/6, N6 in OU. Fundus revealed disc pallor and resolution of macular exudates [Figure 5]. Optical coherence tomography (OCT) macula OU was normal [Figure 4c-f]. She was followed up for 2 years and has had no recurrence till date.Figure 1: Images (a) and (c) showing central scotoma. Images (b) and (d) showing resolution of central scotoma with nonspecific defectsFigure 2: Disc edema with splinter hemorrhages, tortuosity of veins, hard exudates in incomplete macular fan configuration in both eyes with subfoveal hard exudates (black arrow) and arteriolar sheathing (yellow arrows) close to disc in the right eyeFigure 3: (a). Magnetic resonance imaging of brain enhanced with gadolinium contrast showing conglomerate ring-enhancing lesions in the left frontoparietal lobe (indicated by white arrow) with reactive dural thickening. Image (b) with an arrow showing cavitation and image (c) showing centrilobular nodules with a tree in bud appearance suggestive of tuberculosisFigure 4: (a), (d) OCT through disc showing disc edema. (b), (e) Attached macula with peripapillary disc elevation. (c), (f) Normal macular contourFigure 5: Resolution of disc edema with pallor and gliosis and exudatesDiscussion Tuberculous optic neuropathy may occur due to direct infection or hypersensitivity reaction and can present as papillitis, optic neuritis, retrobulbar neuritis, optic nerve tubercle, and neuroretinitis.[1] It may be associated with active intracranial, pulmonary, and disseminated TB. Bilateral neuroretinitis is rare; hence, other infectious causes of neuroretinitis like cat scratch disease and leptospirosis should be excluded.[2] Malignant hypertension should be ruled out. The usage of ethambutol in neuroophthalmic TB is controversial due to concerns of drug-induced neuropathy as it can cause optic neuritis, dyschromatopsia, central scotoma, and disc pallor.[3] It is challenging to monitor toxicity in the setting of preexisting optic neuropathy; hence, an ethambutol-sparing regimen can be considered.[4] Retinal ganglion cell thickness in OCT, patterned visual evoked potentials, contrast sensitivity, and multifocal electroretinogram are sensitive tests, which may help us predict toxicity at subclinical levels.[5] The patient was instead started on injectable second-line ATT drug amikacin, which is normally reserved for patients with multidrug resistance. Appropriate monitoring for ototoxicity and nephrotoxicity was done during the treatment regimen.[6] Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.