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RCOphth Annual Congress 2026
18 - 21 May, 2026 | Manchester Central, Manchester
P032
Atypical Giant Cell Arteritis Causes Bilateral Vision Loss Despite Normal Inflammatory Markers and Negative Ultrasound
Poster Presenter
Authors
Part of Topic
Case reports
Audio
Introduction
In suspected giant cell arteritis (GCA), treatment decisions must prioritise clinical suspicion over reassuring investigations [1].
We present a case of bilateral arteritic anterior ischaemic optic neuropathy occurring in the setting of low-grade inflammatory markers and a negative temporal artery ultrasound, reinforcing that diagnosis in GCA remains fundamentally clinical.
Timeline
Week 0: Initial Assessment
79-year-old Female
• Progressive bilateral painless vision loss (4 weeks)
• VA 6/5 (right), 6/6 (left) to 6/60 bilaterally
• Headache + proximal girdle pain initially misattributed
• Jaw pain not initially recognised as claudication
• CRP 5.9 mg/L, ESR 37 mm/hr, and platelets 422 ×10⁹/L
• MRI unremarkable
Week 3: Ongoing Concern
• Temporal artery ultrasound negative
• Jaw claudication confirmed
• No alternative diagnosis identified.
Week 11: Ischaemia Identified
• Thickened, non-pulsatile temporal artery
• FFA: Marked delayed choroidal filling, supporting arteritic AION
• IV methylprednisolone initiated
Week 16+: Diagnosis
• Temporal artery biopsy: Positive
• Subsequent systemic vascular instability, supporting wider vasculitic burden
Discussion
Why is this case important?
• High clinical probability of GCA (GCAPS >10) at presentation
• Bilateral vision loss and red flag features present
• Corticosteroid initiation was significantly delayed
Diagnostic tension
• Headache and polymyalgia initially attributed to chronic disease/MSK pathology
• Jaw pain not recognized as claudication early
• Inflammatory markers were only mildly elevated
• Negative temporal artery ultrasound provided false reassurance
What the literature says
• ESR, CRP and platelets may be normal or mildly elevated in biopsy-proven GCA cases [2]
• Ultrasound sensitivity is variable and operator dependent [1]
• Temporal artery biopsy remains the diagnostic gold standard [1]
• Delayed choroidal filling on FFA reflects posterior ciliary artery hypoperfusion and supports arteritic disease
• Visual loss is often sudden and irreversible
Key reflection
• GCA remains a clinical diagnosis
• Negative investigations do not exclude disease
• Treatment should not be delayed when clinical suspicion is high
Conclusion
Negative ultrasound and low-grade inflammatory markers do not exclude GCA in high-risk patients (GCAPS ≥10).
Diagnosis remains clinical.
Key actions:
- Start corticosteroids immediately when GCA is suspected with visual symptoms
- Do not delay treatment for confirmatory testing
- Urgent fast-track rheumatology referral is required
This case highlights how over-reliance on investigations can delay treatment and contribute to irreversible visual loss.
References
1. Bilton EJ, et al. Eye. 2023;37:2365–73.
2. van der Geest KSM, et al. JAMA Intern Med. 2020;180:1295–304.
3. Laskou F, et al. Clin Exp Rheumatol. 2019;37(Suppl 117):104–8.