The case is a 28-year-old Chinese male with no past medical or psychiatric history presenting with complaints of constant "static" in his entire field of vision which he subsequently described as "a subtle overlay of an out-of-signal TV screen over my entire vision." Symptoms began shortly following diagnosis with COVID-19 infection. The patient developed symptoms of COVID-19 (fever, cough, loss of sense of taste, and smell) on March 12, 2020, and was confirmed positive for COVID-19 via nasopharyngeal swab on March 20, 2020, by way of a nasopharyngeal swab tested for the coronavirus with reverse transcription-polymerase chain reaction RNA testing. He was subsequently hospitalized for 2 days and treated with IV azithromycin and hydroxychloroquine. The patient was discharged home and eventually tested negative for COVID-19 on April 11, 2020, also via nasopharyngeal swab and RNA, RT PCR. He then reported associated photophobia and palinopsia (after images). He denied prior visual symptoms prior to COVID-19 infection. He was also found to have decreased vision in the left eye by his optometrist and was referred for further evaluation.
The patient presented with best-corrected visual acuity (BCVA) of 20/20 in both eyes (OU). Intraocular pressure (IOP) was 17 mmHg in the right eye (OD) and 16 mmHg in the left eye (OS). Confrontation visual field was full, extraocular motility intact, and pupils equal reactive and reactive to light. Slit lamp exam (SLE) was with clear lens OU and with rare to trace white blood cells (WBCs) in the vitreous OU, but otherwise unremarkable. The cells were only noted with complete darkness and the slit beam and patient inspection of the vitreous over several minutes. Dilated fundus exam (DFE) was without posterior vitreous detachment (PVD) and retinal tear/break/hole, and the cup to disc (c/d) ratio was 0.6 OD and 0.7 OS (shown in Figures 1(a) and 1(b)). Optical coherence tomography (OCT) of the macula showed mild macular thickening OS (shown in Figures 2(a) and 2(b)). OCT retinal nerve fiber layer (RNFL) analysis showed RNFL thickening OD > OS. Fluorescein angiography (FA) studies showed no overt signs of retinal vascular leakage, but subtle staining of retinal vessels and subtle hyperfluorescence of the disc were present. The Octopus 30-2 visual field showed diffuse suppression OU (shown in Figure 3). Given the subtle inflammatory changes on clinical exam and diagnostic imaging, he was trialed on topical bromfenac 0.075% twice daily (BID) OU.
At a subsequent visit, ancillary tests confirmed retinal and optic nerve dysfunction including an electrooculogram (EOG) which showed suppression OD and borderline suppression OS with an Arden ratio of 1.41 (OD) and 1.85 (OS) (shown in Figure 4). Visual evoked potential (VEP) demonstrated mild suppression (shown in Figure 5). Handheld flash electroretinogram (ERG) showed mild to moderate delayed implicit time with reduced photopic negative response OU (shown in Figure 6). The patient underwent laboratory testing with ACE, HLA-B27, ANA, lysozyme, CRP, rheumatoid factor, HIV 1 and 2, ESR, syphilis Ab IgG, QuantiFERON Gold, mitogen, TB1 Ag, TB2 Ag, and CBC, all of which were negative for another cause of ocular inflammation or visual symptoms. Follow-up examination at one month showed decreased retinal thickness consistent with improved posterior segment inflammation but some mild persistent rare cells in the vitreous, and a final follow-up visit three months later revealed resolution of inflammatory cells, stable retinal thickness, and no change in the visual symptoms.
Magnetic resonance imaging (MRI) of the brain and orbits with and without contrast identified mild sinus disease and an incidental 1.6 cm by 1.7 cm arachnoid cyst in the left anterior temporal region. Orbits were unremarkable, and optic nerve was negative for perineural contrast enhancement (shown in Figure 7). The patient was also seen by a neuroophthalmologist who initially diagnosed the patient with presumed optic neuritis in the left eye despite negative MRI findings but, on follow-up, confirmed the diagnosis of visual snow given the absence of ocular inflammation and other pathology that could account for his symptoms.
The patient did report subjective improvement in symptoms with compliance with topical bromfenac and subjective worsening without the use of the topical bromfenac. Symptoms of "static" persisted on follow-up despite resolution of vitreous cells and a normal ophthalmologic exam. Symptoms continue to date of writing, which is more than ten months since the onset of symptoms.