Orbital and ocular perfusion in thyroid eye disease

Abstract

Thyroid eye disease (TED) is characterized by enlargement of extraocular muscles, an increase in retrobulbar fat, orbital fibrosis, and fluctuations in plasma thyroid hormone levels in most patients, often associated with raised autoantibody titers. The occurrence of orbital space conflict compromises the orbital perfusion, unchecked progression of which results in irreversible loss of visual acuity and visual fields. The quantitative assessment of orbital perfusion can be done by measurement of blood flow velocities in the superior ophthalmic vein (SOV), ophthalmic artery (OA), central retinal artery (CRA), and posterior ciliary artery by color Doppler imaging. The retinal and choroidal microvasculature is studied by optical coherence tomography and optical coherence tomography angiography. The orbital and ocular perfusion fluctuates during the course of TED. Orbital congestion is reflected by the reduction or reversal of SOV flow and an increase in subfoveal choroidal thickness. The active phase is characterized by high blood flow velocities of the OA and CRA. The onset of dysthyroid optic neuropathy is associated with reduced arterial perfusion and reduction in parafoveal and peripapillary vascular density. Orbital decompression improves the SOV flow and decreases the resistivity index of CRA. Sequential evaluation of orbital hemodynamic changes can thus supplement the clinical scoring systems for monitoring and planning intervention in TED.

Keywords: Biomarkers; Color Doppler imaging; OCTA; Perfusion; Thyroid eye disease; Thyroid orbitopathy.