A 22-year-old female was admitted through emergency with sudden onset severe headache, vomiting, and dimness of vision (6/60) in both eyes. She was diagnosed with systemic lupus erythematosus one year ago by clinical and laboratory criteria (ACR) with nephropathy grade three. She had been given pulse cyclophosphamide 1 year earlier (6 doses, 21 days apart each). After that, she was put on oral steroids (prednisolone, 7.5 mg/day oral) and she continued the drug in the intervening period. At the time of admission she was still on oral steroids (7.5 mg/day). She had no other manifestations of lupus and her mental status was normal. She also had no prior visual problems.
After admission, the patient developed low grade fever and her dimness of vision progressed. By third day, she had no perception of light in either eye. Local examination of the eyes showed pupils to be dilated and non-reactive. Ophthalmoscopy showed mild papilledema bilaterally. No neck rigidity was elicited. There was bilateral sixth cranial nerve weakness; but no other neurological signs. Ophthalmologists opined that the pathology was not intra-ocular; neurologists were of the opinion that there was a vascular event in cranium. Immediate imaging was advised.
Routine laboratory tests showed mild anemia and thrombocytopenia. Her blood glucose was raised (fasting=144 mg/dL), probably due to long intake of steroids. Due to the presence of papilledema, we did a CT scan of brain [Figure 1] which showed a calcified mass in suprasellar region with perilesional edema (black arrow) with obstructive hydrocephalous. There was also mild cerebral atrophy. The Mantoux test of the patient was negative (she was on steroids), sputum did not show any acid-fast bacilli and chest X-Ray was also normal. She had contact with a sputum positive case of tuberculosis 3 months ago. Her hormonal profile was normal. We could not attempt a spinal tap due to hydrocephalous. The Magnetic resonance imaging scan could not be done due to cost factor. In view of the emergent nature of the illness, we started her on oral anti tubercular drugs with an increased dose of oral steroids. Her headache decreased, but vision improved only mildly. Subsequently, after 1 month, a brain biopsy was done and the lesion was found to be calcified granuloma with aggregates of epitheloid cells, calcifications, necrosis, blood vessel destructions, and few scattered caseations [Figure 2]. The lesion did not show any acid fast bacilli, but overall features were suggestive of tuberculosis. A CSF sample collected at time of brain biopsy showed increased cells (45/muL), increased protein (102 mg/dL). AFB stain of CSF was negative; a PCR from CSF was positive for mycobacterium tuberculosis. Repeat CT scan [Figure 3] showed only a mild decrease in the size of the edema; calcified mass size was the same. She was put on anti-tubercular drugs for 1 year. At present her vision is finger counting at three feet.