Semaglutide dose escalation linked to atypical retrobulbar optic neuropathy in a patient

Semaglutide, a GLP-1RA, is a cornerstone therapy for type 2 diabetes and obesity, offering significant glycemic control and weight loss benefits. While its efficacy is well-established, post-marketing surveillance has identified a signal for nonarteritic anterior ischemic optic neuropathy (NAION) in some users. This particular case, however, highlights an important distinction: a retrobulbar presentation, which is anatomically and clinically distinct from NAION and warrants specific attention due to its atypical nature and potential implications for patient monitoring.

This report details a single case study of a patient who developed visual disturbances following semaglutide dose escalation. The patient's clinical course was meticulously documented, focusing on the onset of symptoms, the specific nature of the visual impairment, and the temporal relationship with the semaglutide dosage adjustments. The primary intervention was the immediate discontinuation of semaglutide upon diagnosis of the optic neuropathy, followed by serial ophthalmological follow-up to monitor visual function and assess any progression or resolution of symptoms.

The patient experienced an atypical retrobulbar optic neuropathy, specifically manifesting as a persistent left central scotoma, in close temporal proximity to the semaglutide dose escalation.

Upon immediate discontinuation of semaglutide, the patient's visual function stabilized, showing no further deterioration during subsequent follow-up examinations. This stabilization allowed for adaptation to the persistent scotoma, indicating that the progression of the neuropathy halted once the suspected causative agent was removed. The presentation was deemed "atypical" due to its retrobulbar nature, differentiating it from the more commonly reported NAION associated with GLP-1RA use, suggesting a potentially distinct pathophysiological mechanism or a broader spectrum of ocular adverse events.