Bilateral corneal endothelial failure following COVID-19 pneumonia

Abstract

We describe a patient who developed acute bilateral corneal decompensation following COVID-19 pneumonia and prolonged intensive care unit ventilation. SARS-CoV-2 uses human ACE2 as the receptor for entry with subsequent downregulation of ACE2. ACE2 receptors are found in human ocular surface cells including cornea. Mouse models of ACE2 deficiency result in corneal haze, oedema and ocular surface inflammation due to upregulation of the inflammatory cascades. We therefore hypothesise that the cause of this patient's corneal decompensation was viral endotheliitis due to direct infection by the SARS-CoV-2 virus.

Keywords: COVID-19; ophthalmology.