Discussion
Ocular manifestations of SARS-Cov2 in humans are not fully recognized. Previous reports indicated ophthalmic presentations from conjunctivitis and anterior uveitis to retinitis and optic neuritis3.
As shown in previous studies there is an association between SARS-Cov2 infection and hypercoagulability. The SARS-Cov2 binds to the host cells by angiotensin-converting enzyme (ACE)-2 receptor(R). ACE-2Rs are present in high density in the heart, lungs, arteries, and veins. So these organs are more vulnerable to the invasion of the pathogen. SARS-Cov2 causes endothelial dysfunction by binding to ACE-2Rs in retinal and choroidal microvasculature and leads to tissue ischemia, edema, and pre-coagulation state. Besides that, the systemic inflammatory response and cytokines release activates the coagulation cascade which results in venous and arterial thromboembolic complications 2.
Nonarteritic anterior ischemic optic neuropathy (NAION) is caused by infarction of the short posterior ciliary arteries that supply the anterior portion of the optic nerve head. Although the exact pathophysiology of the condition is not recognized some risk factors are noted in the literature including diabetes mellitus, hypercholesterolemia, smoking, anemia, and hypercoagulable state4.
In our patient with a history of diabetes mellitus as a risk factor for AION and a history of COVID-19 infection, it seems that the hypercoagulable state and hypoxia caused by COVID-19 infection predisposed him to NAION.
COVID-19 infection has the potential to cause damage to the choroid, retina, and optic nerve. Increased choroidal thickness, features of pachychoroid and abnormal dilation of Haller’s layer vessels are reported in patients with COVID-19 infection in previous research5. As discussed above it seems that a disturbance in autoregulation of the RAAS system caused by the binding of SARS-Cov2 to ACE-2R results in endothelial dysfunction, increased vascular permeability, dilatation of retinal and choroidal vessels. Changes in the retinal and optic nerve head microvasculature have been identified in previous research. A decrease in vessel density (VD) in the superficial and deep capillary plexus, as well as an increase in inner disc small vessel VD which can be associated with optic disc hyperemia and edema, have been documented 6-8. These alterations suggest that COVID-19 infection puts patients at risk for retinal and optic nerve disorders.
In our patient, EDI-OCT revealed increased choroidal thickness. It is supposed that the thickening of the choroid led to anterior rotation of the ciliary body and resulted in a shallow anterior chamber. So that aqueous misdirection occurred and secondary angle-closure glaucoma developed.
NAION is caused by hypoperfusion of the optic nerve. Our patient presented with bilateral NAION in the setting of COVID- 19 infection. Hypoxemia and the hypercoagulable state as the sequence of COVID-19 infection may result in NAION in this patient. Also, increased choroidal thickness in the setting of COVID-19 infection may cause anterior rotation of the ciliary body and secondary angle-closure glaucoma consequently. There are three possible mechanisms for ocular complications in our patients: vascular endothelial damage, hypercoagulable state, and hypoxemia. At present, it is not possible to determine a causal or coincidental relationship between NAION, choroidal hypoperfusion, and secondary angle-closure glaucoma that occurred in described patient and COVID-19 infection. But the purpose of this report is to shed light on the potential and multiplicity of ophthalmic presentation in a patient with COVID-19 infection.