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.