Vision loss in giant cell arteritis: case-based review
Ioanna Nefeli Kokloni1, Souzana Ioanna Aligianni1, Olga Makri2
1Medical Graduates, University of Patras Medical School, Patras, Greece.
Insights
Prompt glucocorticoid treatment for giant cell arteritis (GCA) is crucial. Even with treatment, sequential blindness in the fellow eye can rarely occur, emphasizing the need for immediate intervention to preserve vision.
Area of Science:
- Ophthalmology
- Rheumatology
- Neurology
Background:
- Giant cell arteritis (GCA) is a vasculitis that can cause vision loss.
- Prompt glucocorticoid treatment is recommended for suspected or proven GCA with visual symptoms.
- Pulse therapy aims to prevent involvement of the unaffected fellow eye.
Observation:
- A case of biopsy-proven GCA in a 79-year-old man resulted in sequential bilateral blindness.
- Despite initial intravenous methylprednisolone and oral prednisone, the second eye lost vision 11 days after initial unilateral vision loss.
- A systematic literature search identified 21 additional patients with GCA experiencing contralateral vision loss under pulse treatment for monocular vision loss.
Findings:
- Contralateral vision loss occurred 1-12 days after treatment initiation (median 2 days).
- Treatment initiation was delayed up to 8 days from initial vision loss (median 2 days).
- Anterior ischemic optic neuropathy was the primary cause of vision loss.
Implications:
- Sequential involvement of the fellow eye in GCA-related vision loss is rare but can occur.
- While the first 2 days are critical, vision loss can happen later.
- Immediate initiation of pulse glucocorticoid treatment is vital for preserving vision in the contralateral eye.
Abstract:
Prompt initiation of pulse glucocorticoid treatment is recommended in case of visual symptoms and suspected or proven giant cell arteritis (GCA). Pulse treatment in most cases prevents involvement of an initially unaffected fellow eye. We present the case of a biopsy-proven GCA in a 79-year-old man, complicated by sequential bilateral blindness. Initial unilateral vision loss was treated by 1 g methylprednisolone intravenously for 3 days, followed by 1 g/kg prednisone daily. Despite treatment, the second eye went completely blind 11 days after the initial vision loss. We performed a systematic search on Medline and Scopus aiming at identifying all cases of GCA complicated with loss of vision in a previously unaffected eye under pulse treatment for initially monocular vision loss. We identified 11 articles reporting 21 patients that met our inclusion criteria. Contralateral vision loss occurred 1-12 days following treatment initiation, with a median of 2 days. Treatment initiation was delayed up to 8 days since the initial vision loss, with a median delay of 2 days. Anterior ischemic optic neuropathy was the dominant mechanism of vision loss. Sequential involvement of the fellow eye in case of unilateral vision loss in GCA is rare. With 12-day interval being the longest reported, we conclude that even though the first 2 days are the most critical for the visual outcome, blindness in the initially unaffected eye may rarely occur later. Nonetheless, immediate initiation of pulse treatment remains of vital importance to preserve vision in the contralateral eye.
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