To the Editor:

We read the article correlating the structural changes in the retina with the severity of thyroid eye disease (TED) with great interest. The authors highlighted the importance of close monitoring of the ganglion cell layer/inner plexiform layer (GCL/IPL) in moderate to severe TED to detect subclinical atrophy of the optic nerve [1].

The authors divided the cases into mild, moderate-to-severe, and Dysthyroid optic neuropathy (DON) categories [2]. The amount of proptosis, however, appears to overlap between the groups, and for a clearer depiction, data should have been presented in terms of confidence intervals. The exophthalmometry readings vary in different races, and the addition of control group readings would be desirable.

Though the study mentions thinning trend of GCL/IPL in moderate-to-severe TED as an indication for orbital decompression on the basis of single readings, the study fails to elicit the critical values for surgical intervention [1]. Twenty-eight of 75 cases had received steroids and none of the 42 eyes in the moderate-to-severe group had CAS > 3. A correlation with the duration of the disease would have given an insight into the cause of clinical inactivity in these cases. Also, a generalized decrease of GCL in all the cases of moderate-severe TED reflects the possibility of lack of appropriate steroid therapy, which has led to optic nerve damage.

The reduction in GCL/IPL thickness strongly correlates with reduced vascularity in the parafoveal superficial and deep capillary plexuses [3]. The orbital blood flow also shows a higher resistivity index of the ophthalmic artery and central retinal artery and a decrease in arterial end-diastolic velocities in DON [4].

Since ocular coherence tomography (OCT), OCT Angiography, and Colour Doppler ultrasonography are non-invasive investigations, adding these to the armamentarium can play an adjunctive role in the detection of early optic nerve ischemia.