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.
