Optic Nerve Infarction in a Patient With Coronavirus Disease 2019.

Abstract

Severe acute respiratory syndrome 2 (SARS-CoV2), also called coronavirus disease 2019 (COVID-19), has spread worldwide and affected millions of lives. Although there are many unaddressed questions about the pathogenesis of the virus and the best treatment, it is known that the virus affects several organ systems, including respiratory, gastrointestinal, and neurologic (1–4). Neurologic manifestations reported in COVID-19 patients include headache, anosmia, seizure, stroke, encephalitis, and Guillain–Barre syndrome (4); However, neuro-ophthalmic manifestations have infrequently been reported (5–8). We describe a patient with COVID-19 who developed thrombosis of the left internal carotid artery leading to infarction of the left optic nerve. A 50-year-old man was found to have a positive polymerase chain reaction (PCR) test for COVID-19. Twelve days later, he developed fever, cough, and dyspnea. His respiratory symptoms worsened, and 2 days later, he was admitted to hospital for acute onset of aphasia and right hemiparesis. After computed tomography (CT) of the brain excluded a hemorrhagic stroke, the patient was given intravenous tissue plasminogen activator and referred to our medical center. His medical history included poorly controlled diabetes mellitus, hypertension, and hyperlipidemia. On admission, the patient was lethargic, oriented to self, aphasic, and not following commands. He had right hemiplegia and left gaze preference. Nasal and oropharyngeal swabs for real-time PCR confirmed infection with SARS-CoV2, and due to his respiratory failure, he was intubated and transferred to the intensive care unit. His hematologic studies included white blood cells of 12.6 × 103/µL (normal, 4–11/µL) with 4% lymphocyte (normal, 15%–52%), C-reactive protein 214 mg/L (normal, 0–10.9 mg/L), d-dimer >20,000 ng/mL (normal, 0–240 ng/mL), lactate dehydrogenase 280 U/L (normal, 120–240 U/L), and fibrinogen 1,228 mg/dL (normal, 220–498 mg/dL). Neuroimaging studies were obtained. CT angiography (CTA) was consistent with occlusion of the cervical and intracranial portion of the left internal carotid artery (Fig. 1). Subsequent brain MRI demonstrated scattered acute infarcts in the distribution of the left middle cerebral artery. Diffusion-weighted imaging (DWI) showed restricted diffusion along the intraorbital portion of the left optic nerve (Fig. 2).FIG. 1.: CTA. Sagittal and axial images reveal total occlusion of the left internal carotid artery (A, arrow) and absent flow in the artery at the skull base (B, arrow).FIG. 2.: A. Diffusion-weighted scan shows multiple areas of ischemia in the left cerebral hemisphere. B. Diffusion-weighted scan demonstrates restricted diffusion in the left intraorbital optic nerve (arrow). C. The apparent diffusion coefficient (ADC) map confirms restricted diffusion of the left optic nerve (arrow).After 3 weeks, as the patient's respiratory condition and mental status improved, he reported loss of vision in his left eye. At that time, visual acuity was 20/50 in the right eye and no light perception in the left eye. There was a left relative afferent pupillary defect, eye movements were intact, and the fundi were unremarkable. Six weeks later, visual function was unchanged, but the left optic disc was now pale. Cerebrovascular ischemia is a recognized complication of the COVID-19. A series of 219 patients with COVID-19 from Wuhan, China, revealed a 4.6% rate for acute ischemic stroke (1). In this series, patients with COVID-19 who developed stroke were significantly older than non-COVID-19 stroke patients (75.7 ± 10.8 vs 52.1 ± 15.3 years) and had other cardiovascular risk factors. In contrast, Oxley et al (2) reported 5 patients younger than 50 years with COVID-19 who were diagnosed with acute stroke; 2 had no cardiovascular risk factors. Our patient had several risk factors for stroke, including diabetes mellitus, hypertension, and hypercholesterolemia. The mechanism of thromboembolic events in COVID-19 is controversial. Connor and colleagues (3) suggested that a contributing factor is the elevated level of coagulative factors, including platelet, fibrinogen, and d-dimer. Vascular endothelial dysfunction that impairs its antithrombotic properties is another proposed mechanism (4). There are few reports of visual loss associated with COVID-19 disease. Four patients have been documented with profound visual loss due to bilateral parieto-occipital or bilateral occipital lobe infarctions (5–7). In addition, Zhou et al (8) described a patient with COVID-19 who developed bilateral myelin oligodendrocyte glycoprotein (MOG)–associated optic neuritis. The authors speculated that COVID-19 provided a “potential connection” between the viral disease and central nervous system demyelination. DWI in our patient demonstrated acute infarction of the intraorbital portion of the left optic nerve due to thrombosis of the left internal carotid artery. Our report expands the spectrum of neuro-ophthalmic findings in patients with COVID-19.