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Central nervous system tuberculosis presenting as branch retinal vein occlusion Clin Exp Optom 2013; 96: 121–123 Nikolaos Kopsachilis MD Manpreet Brar MD Anca IC Marinescu MD Richard Andrews MD Moorfields Eye Hospital, London, United Kingdom E-mail:
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DOI:10.1111/j.1444-0938.2012.00757.x Branch retinal vein occlusion (BRVO) associated with ocular tuberculosis (TB) is a rare presentation of retinal vasculitis but it can also present in the absence of active uveitis. We present a 39-year-old patient with BRVO who slowly developed bilateral papilloedema due to TB in the central nervous system. To our knowledge, this is the first case of systemic central nervous system TB confirmed by biopsy presenting as a branch retinal vein occlusion and shows the importance of extensive causative investigation of BRVO, especially for young patients.
Submitted: 7 December 2011 Revised: 19 March 2012 Accepted for publication: 17 April 2012
Key words: branch retinal vein occlusion, ocular tuberculosis, papilloedema
Intraocular tuberculosis is a rare condition caused by Mycobacterium tuberculosis or Mycobacterium bovis and represents one per cent of all cases of systemic tuberculosis (TB).1 There are few unmistakable features of intraocular TB. When it does occur, the most common features are anterior or posterior uveitis including retinal vasculitis or neuroretinitis but these features occur in many other conditions, such as serpiginous-like choroiditis,2 sarcoidosis, toxoplasma, syphilis or viral infection, making diagnosis difficult. Although there have been few reports of retinal vasculitis causing retinal vein occlusion associated with ocular tuberculosis,3 it is very rare for it to present in the absence of uveitis.4 To our knowledge, this is the first case of systemic central nervous system tuberculosis confirmed by biopsy
and presenting as branch retinal vein occlusion (BRVO).
CASE REPORT A 39-year-old man from Pakistan was referred to our clinic with sudden deterioration of vision in his left eye. The patient admitted to have frequent travels to his homeland in the last two years. No systemic diseases or general complaints, such as cough, headaches, joint pains or fever were recorded. Visual acuity (VA) was 6/6 in the right eye and 2/60 in the left eye. Intraocular pressure was 13 mmHg in both eyes. Slitlamp examination showed a deep anterior chamber in both eyes with no signs of acute, chronic or previous inflammation.
© 2012 The Authors Clinical and Experimental Optometry © 2012 Optometrists Association Australia
Fundoscopy of the left eye revealed an infero-temporal BRVO with multiple flame-like haemorrhages, macular oedema and cotton wool spots. No vitreous cells were noted. The right fundus appeared normal. Fluorescein angiography of the left eye showed blockage corresponding to the areas of haemorrhage with exudation and late leakage. The site of the occlusion seemed to be at an arterio-venous crossing. Blood pressure and glucose were within normal limits. Full serology was investigated. Full blood count, erythrocyte sedimentation rate and C-reactive protein were normal. Further blood investigation failed to show evidence of homocystinuria, rare blood coagulopathies, sarcoidosis, toxoplasmosis, HIV or syphilitic infection. Tuberculin sensitivity test measured Clinical and Experimental Optometry 96.1 January 2013
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Branch retinal vein occlusion in CNS tuberculosis Kopsachilis, Brar, Marinescu and Andrews
One month after beginning isoniazid, visual acuity remained at 6/6 in the right eye and improved to 6/24 in the left, with marked resolution of the papilloedema in both eyes. Repeat fluorescein angiogram was negative for any vasculitis process.
DISCUSSION
Figure 1. Fundus photographs of patient’s right and left eyes three weeks after diagnosis of a branch retinal vein occlusion in the left eye. (A) Right eye showing severe papilloedema. (B) Left eye showing multiple retinal haemorrhages with macular oedema and cotton wool spots. No visible vitreous cells or infiltrates could be detected. (C, D) Fluorescein angiography of right and left eyes revealing an ischaemic branch retinal vein occlusion in the left eye. The occlusion seems to be at an arterio-venous crossing.
6.0 mm and was found to be nonindicative of active tuberculosis. Rheumatoid factor and antinuclear antibodies were negative. Chest X-ray was normal. Six weeks later, optic disc swelling was detected in both eyes and the patient reported persistent headache. Right VA was 6/6 and left VA was 1/60. No signs of intraocular inflammation were detected (Figure 1). A cranial computed tomography (CT) scan was performed urgently and showed symmetrical white matter hypodensity and swelling of the posterior temporo-parietooccipital regions, as well as symmetrical gyriform thickening and hyperdensity of the cortex overlying the occipital lobes (Figure 2). Magnetic resonance imaging was performed and confirmed that these changes were compatible with an infective aetiology and less likely to be an intracranial neoplasm (Figure 2). Clinical and Experimental Optometry 96.1 January 2013
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Further virology tests for herpes, varicella and cytomegalovitus immunoglobulin M (IgM) antibodies were negative. The patient was referred to our neurology department. A diagnostic lumbar puncture was performed and showed normal opening pressure, elevated protein levels, low glucose and no growth in cerebrospinal fluid cultures. Further clinical examination revealed enlarged cervical and submandibular lymph nodes and a biopsy showed a core of lymphoid tissue with caseating epithelioid granulomas and scattered Langhan’s giant cells, confirming the diagnosis of TB. The patient was commenced on anti-TB treatment with ethambutol (1.0 g), isoniazid (300 mg), rifampicin (600 mg) and pyrazinamide (1.5 g) for two months, followed by maintenance therapy of isoniazid and ethambutol for four months.
Branch retinal vein occlusion associated with ocular tuberculosis is a rare presentation of retinal vasculitis3 but it can also present in the absence of active uveitis.4 In our case report a young patient, who frequently travelled to Asia, presented with BRVO and slowly developed bilateral papilloedema due to TB in the central nervous system. In this case, the slow evolution of TB was clearly illustrated by the later development of lymphadenopathy. There was no pulmonary or other systemic involvement. With regards to the pathophysiology, we assume that Mycobacteria spread to the choroid, mainly by haematogenous routes and caused a mechanical compression or blockade of the retinal vessels, thus leading to BRVO. This hypothesis could be supported by the absence of any signs of vasculitis or uveitis in our patient, the development of bilateral papilloedema and the fact that the occlusion seemed to be at an arterio-venous crossing. Of course, it is also possible that the patient had a vein occlusion secondary to unrecognised retinal vasculitis. This can be presumed by looking at the late coloured photograph (Figure 1B) where the vein does appear whitish; however, in the corresponding fluorescent images (Figure 1D), there are no signs of vasculitis. This rare presentation of systemic TB shows the importance of extensive causative investigation of BRVO, especially for young patients.5 Differential diagnoses should always include other infectious, systemic conditions (including diabetes, hypertension, collagenosis, Behçet’s disease and sarcoidosis) and hypercoagulable aetiology with a weighting for the patient’s age. © 2012 The Authors
Clinical and Experimental Optometry © 2012 Optometrists Association Australia
Branch retinal vein occlusion in CNS tuberculosis Kopsachilis, Brar, Marinescu and Andrews
Figure 2. Cranial computed tomography of a patient three weeks after diagnosis of a branch retinal vein occlusion with bilateral papilloedema. (A) Transverse section showing symmetrical gyriform thickening and hyperdensity of the cortex overlying the occipital lobes (white arrows). (B) Coronal section showing symmetrical white matter hypodensity and swelling of the posterior temporo-parieto-occipital regions (white arrows). Magnetic resonance imaging (MRI) confirmed that these changes were compatible with an infective aetiology and less likely for an intracranial neoplasm. (C) Transverse section MRI and (D) coronal section MRI of the same patient.
Treatment in a patient with choroidal vasculitis with a secondary retinal obstruction due to TB should include isoniazid 5 mg/kg/day, rifampicin 600 mg/day, ethambutol 15 mg/kg/day and pyrazinamide 20 mg/kg/day for the first four months followed by rifampicin and isoniazid for 9–14 months.6 Summarising, we report an unusual presentation of a BRVO as a result of systemic central nervous system TB and emphasise the need for thorough systemic evaluation in young patients with BRVO.
2. Mackensen F, Becker MD, Wiehler U, Max R, Dalpke A, Zimmermann S. QuantiFERON TBGold—a new test strengthening long-suspected tuberculous involvement in serpiginous-like choroiditis. Am J Ophthalmol 2008; 146: 761–66. 3. Gupta A, Gupta V, Arora S, Dogra MR, Bambery P. PCR positive tubercular retinal vasculitis: clinical characteristics and management. Retina 2001; 21: 435–444. 4. Fullerton DG, Shrivastava A, Munavvar M, Jain S, Howells J, Macdowell P. Pulmonary tuberculosis presenting with central retinal vein occlusion. Br J Ophthalmol 2007; 91: 1714–1715. 5. Gupta A, Agarwal A, Bansal RK, Agarwal A, Chugh KS. Ischaemic central retinal vein occlusion in the young. Eye 1993; 7: 138–142. 6. Rosen PH, Spalton DJ, Graham EM. Intraocular tuberculosis. Eye (Lond) 1990; 4: 486–492.
REFERENCES 1. Bouza E, Merino P, Muñoz P, Sanchez-Carrillo C, Yáñez J, Cortés C. Ocular tuberculosis. A prospective study in a general hospital. Medicine (Baltimore) 1997; 76: 53–61.
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