Case presentation:
A 38-year-old female presented to the emergency in our hospital with history of headache and blurry vision. Her past medical history was significant for diabetes mellitus, obstructive sleep apnea, migraine, gastritis, and obesity. Her last hospital admission was two weeks ago, due to COVID-19 pneumonia. She was admitted for ten days and treated as our local guideline with azithromycin, hydroxychloroquine for 7 days, and amoxicillin-clavulanic acid. Her COVID-19 infection course was mild in nature as she only needed oxygen supplementation for 4 days. Regarding this admission, she described headache that increased gradually in severity since she was discharged, more severe in the morning, increase with straining, and awaken her from sleep and most importantly it is different from here usual migraine episodes. This headache was followed by blurry vision that worsened gradually over one week and difficulty distinguishing colors especially in the left eye as well as painful eye movements. She experienced nausea few times but no vomiting. Initial vitals were normal with temperature of 36.8 °C, respiratory rate of 19 breaths per minute, blood pressure of 145/80mmHg, oxygen saturation of 99%, and weight of 117.3 kg. Ophthalmology examination showed severe optic disc swelling on the left and mild on the right side, color vision 1/7 in the left eye and 7/7 in the right. Labs were only remarkable for microcytic anemia. COVID-19 PCR was negative on current admission. CT head revealed slightly bulky left optic nerve with optic disc swelling without CT evidence of acute intracranial abnormality. Here, the patient was admitted to the inpatient medical ward with a clinical picture of idiopathic intracranial hypertension. Lumbar puncture (LP) revealed an opening pressure of 45 cm H2O, and 40 mL clear and colorless CSF was drained at this time. With evidence of increased intracranial pressure by LP findings, acetazolamide 250 mg TID was initiated. After that, the patient reported mild improvement in her headache but her visual acuity remained the same. We decided to monitor her for few days for possible improvement, in the fourth day as her vision still deteriorated. Another LP was performed which revealed normal opening pressure of 18 cmH2O with normal CSF analysis. MRI bilateral orbit (Figure 1) revealed effacement of the perioptic optic CSF space, mild diffuse increased T2 signal principally involving the of optic nerve entire intra-orbital segment extending anteriorly to the papilla, with mildly raised optic disc, showing significant diffusion restriction on DWI series and post contrast optic nerve and perioptic enhancement with mildly raised enhancing papilla/ optic nerve insertion.
Above described appearances are suggestive of possible acute inflammatory versus demyelinating process (NMOSD) of the optic nerve on both sides. The bilateral involvement as well as the extent of involvement are suggestive of anti-MOG optic neuritis. There were no findings suggesting ischemic optic neuropathy or increased intracranial tension.
MRI orbit results raised our suspicion that it might be COVID-related post-infectious optic neuropathy due to her history of recent COVID-19 infection. At this point we decided to start IV methylprednisolone for 5 days course and acetazolamide dose was increased to 500mg BID. Aquaporin-4 antibodies and oligoclonal bands were negative. Despite a 7-day course of steroids, the patient reported only mild improvement in vision. However, visual acuity regressed after completion of course of steroids. She was started on plasma exchange for further management; however, she developed anaphylactic reaction and thus, plasma exchange was aborted. Her serum IgA level assessed prior to plasma exchange was normal. She then received a trial of intravenous immunoglobulin (IVIG) for 5 days after which she reported significant improvement in her visual acuity and she was discharged home.