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.