How can giant cell arteritis be diagnosed without a temporal artery biopsy in a patient aged ≥50 years presenting with new-onset temporal headache, scalp tenderness, jaw claudication, visual disturbances, polymyalgia rheumatica‑type proximal muscle pain, and elevated erythrocyte sedimentation rate and C‑reactive protein?

Diagnosing Giant Cell Arteritis Without Biopsy

Giant cell arteritis can be diagnosed without temporal artery biopsy using vascular imaging (temporal artery ultrasound, MRI, CT angiography, or FDG-PET/CT) combined with clinical features and elevated inflammatory markers, though biopsy remains the gold standard when feasible. 1, 2

Clinical Diagnostic Approach

High-Yield Clinical Features (Likelihood Ratios)

The following clinical findings substantially increase the probability of GCA and should be systematically assessed:

• Limb claudication (LR+ 6.01) – the strongest clinical predictor 1, 2
• Jaw claudication (LR+ 4.90) – present in approximately 50% of patients 1, 2, 3
• Temporal artery thickening on palpation (LR+ 4.70) 1, 2, 3
• Loss of temporal artery pulse (LR+ 3.25) 1, 2, 3
• Temporal artery or scalp tenderness (LR+ 3.14) 1, 3
• Age >70 years increases likelihood (negative LR 0.48 when absent) 1, 3

Essential Laboratory Markers

Both ESR and CRP must be obtained as they provide complementary diagnostic information: 1, 2

• ESR >100 mm/h (LR+ 3.11) strongly supports GCA 1, 2, 3
• Normal ESR (<40 mm/h) argues strongly against GCA (negative LR 0.18) 1, 2, 3
• Normal CRP (<2.5 mg/dL) argues strongly against GCA (negative LR 0.38) 1, 2, 3
• Platelet count >400 × 10³/μL (LR+ 3.75) supports diagnosis 1, 2

Important caveat: GCA can rarely occur with normal inflammatory markers in 0.8-4% of cases, so clinical suspicion should not be dismissed based solely on normal ESR/CRP 4

Vascular Imaging as Biopsy Alternative

Temporal Artery Ultrasound (First-Line Imaging)

Temporal artery ultrasound performed by experienced operators is the preferred non-invasive diagnostic modality: 1, 2, 5

• "Halo sign" (circumferential wall thickening) has 88% sensitivity and 97% specificity for GCA 1
• Should be performed within days of starting glucocorticoids, as sensitivity decreases with treatment 5, 6
• Can replace biopsy in the context of typical clinical presentation 5
• Advantages: non-invasive, inexpensive, immediate results, high accuracy 4, 6

Large Vessel Imaging (Essential for Complete Evaluation)

All patients with suspected GCA should undergo large vessel imaging to detect extracranial involvement: 1, 2, 5

• MR angiography or CT angiography of neck/chest/abdomen/pelvis evaluates aorta and major branches 1, 2, 5
• FDG-PET/CT detects large vessel vasculitis in approximately 20% of elderly patients with inflammatory syndromes 5
• Large vessel involvement occurs in 38-61% of GCA patients and is more common in those without cranial symptoms 7
• Critical point: One-third of GCA patients have no temporal artery involvement, making large vessel imaging essential for diagnosis 5

When Imaging Replaces Biopsy

Biopsy can be avoided when: 1, 2, 5

• Temporal artery ultrasound shows characteristic "halo sign" in a patient with typical clinical presentation and elevated inflammatory markers 1, 5
• Large vessel imaging (MRI, CT, or PET/CT) demonstrates characteristic circumferential arterial wall thickening or increased FDG uptake in the appropriate clinical context 1, 2, 5
• Imaging must be performed within 2-7 days of starting glucocorticoids to maintain diagnostic sensitivity 1, 2, 5

Diagnostic Algorithm Without Biopsy

1. Assess clinical probability using high-yield features (jaw/limb claudication, temporal artery abnormalities, age >70) 1, 2

2. Obtain ESR, CRP, and platelet count – normal values argue strongly against GCA but do not completely exclude it 1, 2, 3

3. Perform temporal artery ultrasound as first imaging modality if available and operator experienced 5, 6

4. Obtain large vessel imaging (MRA, CTA, or FDG-PET/CT) to evaluate aorta and major branches, especially if:

   • Temporal artery ultrasound is negative but clinical suspicion remains high 1, 2
   • Patient presents without cranial symptoms (constitutional symptoms only) 7
   • Patient has limb claudication or other signs of large vessel involvement 2, 7

5. Start high-dose glucocorticoids (40-60 mg prednisone daily) immediately if clinical suspicion is reasonable – do not delay treatment awaiting imaging or biopsy 1, 2, 3

Critical Pitfalls to Avoid

• Never delay glucocorticoid therapy while awaiting diagnostic confirmation – untreated GCA carries 14-50% risk of permanent vision loss 1, 2, 3
• Do not rely on a single clinical or laboratory feature – no individual finding is sufficient to rule in or rule out GCA 1
• Do not dismiss GCA based solely on normal inflammatory markers – rare cases (0.8%) present with normal ESR and CRP 4
• Do not limit evaluation to temporal arteries – large vessel involvement without cranial symptoms occurs in 22% of patients 7
• Perform imaging within days of starting treatment – sensitivity of all imaging modalities decreases with glucocorticoid therapy 5, 6

Special Populations

Patients without cranial symptoms (22% of GCA cases): 7

• Present with constitutional symptoms alone or extracranial manifestations (limb claudication)
• Have lower inflammatory markers (median CRP 68 vs 120 mg/L)
• Show higher rates of aorta/branch involvement (61% vs 38%)
• Require large vessel imaging for diagnosis since temporal artery evaluation may be negative 7