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Mattie Adams
This 10YO boy was referred for asymptomatic retinal lesions. He was adopted, so the family history was unknown. The patient and guardian reported a longstanding history of persistent diarrhea that at times required hospitalization. Vision was 20/20 bilaterally.
Color photography shows bilateral torpedo-shaped areas of depigmentation in each superotemporal macula. The lesions were hypo-autofluorescent (not shown). OCT scanning shows outer retinal atrophy through each lesion.
Learning Points:
Torpedo maculopathy was originally described by Gass as a solitary hypopigmented nevus of the RPE (Arch Ophthalmology 1992;110:1358-1359). These benign lesions are teardrop-shaped and are almost always located in the horizontal meridian in the temporal macula. Vision is almost always normal. There is a small risk of macular neovascularization.
The lesions are virtually always unilateral, and we found only a single case report of bilateral lesions in a PubMed search (Richez et al., J Fr Ophthalmol 2010;33:296). Given our patient’s GI symptoms and bilaterality, genetic testing was recommended, but he was unfortunately immediately lost to follow-up.
Am J Ophthalmol. 2026 Aug:288:315-324. doi: 10.1016/j.ajo.2026.04.013.
Biopsy-proven GCA: Visual symptoms prompt more rapid Dx and Tx vs nonspecific symptoms — Retrospective, 300 patients
Purpose: To evaluate diagnostic delays in biopsy-proven giant cell arteritis (GCA) within the Veterans Health Administration (VHA), with a focus on the impact of presenting symptoms and provider specialty on time to treatment.
Design: Retrospective, multicenter cohort study.
Subjects: Using the VHA Informatics and Computing Infrastructure, we identified 24,857 patients with GCA-related diagnostic codes or temporal artery biopsy procedures.
Methods: A multistep filtering process, including positive diagnostic coding and pathology-confirmed biopsy report review, yielded 300 cases of biopsy-proven GCA for final analysis. Detailed chart review captured presenting symptoms, initial provider specialty, and diagnostic timeline intervals, including symptom onset to clinical visit and visit to corticosteroid initiation. Group comparisons were assessed using the Kruskal-Wallis test, and post-hoc pairwise comparisons used Dunn’s Test with Bonferroni adjustments.
Main outcome measures: Time from first symptom to initial clinical visit, and time from initial visit to corticosteroid initiation.
Results: The cohort was predominantly male (94.3%) and White (89.9%), with a mean age of 75.3 years. The average delay from symptom onset to first clinical encounter was 22 days (SD: 31.9), and from encounter to treatment initiation was 11 days (SD: 26.0). Patients initially evaluated by emergency department or eye care providers were treated significantly sooner than those seen by primary care. Presenting symptoms influenced timeliness: patients with ocular symptoms, including transient vision loss and visual disturbances, were treated more promptly (mean: 8.3 days from presentation compared to those with headache (12.9 days) or systemic complaints (20.2 days; P < .001). Classic symptoms such as scalp tenderness and temporal pain led to the shortest delays following examination. Inflammatory markers such as erythrocyte sedimentation rate and C-reactive protein were elevated in the majority of cases, while platelet elevation was less frequent.
Conclusions: This is the first national VHA study to evaluate diagnostic delay in biopsy-proven GCA by provider specialty and symptom type. Our findings demonstrate that visual symptoms prompt more rapid diagnosis and treatment, whereas nonspecific symptoms result in significant delays, particularly in primary care settings. These results highlight a need for improved provider education and systematic approaches to recognize and manage GCA in its varied presentations. Early diagnosis remains critical to prevent irreversible vision loss and other complications.
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