Investigations for giant cell arteritis
It is important to note that a thorough clinical assessment remains the gold-standard diagnostic tool for giant cell arteritis; see Clinical features of giant cell arteritis.
Investigations commonly performed for most systemic vasculitides (including giant cell arteritis) are outlined in Investigations for systemic vasculitides.
Inflammatory markers including erythrocyte sedimentation rate (ESR) and serum C-reactive protein (CRP) concentration are commonly raised in patients with giant cell arteritis; however, if the patient has a high pretest probability for giant cell arteritis, normal inflammatory markers do not exclude the diagnosis. Ideally, request the inflammatory markers and review the patient within 24 hours. In rural and remote settings, this may only be possible by referring the patient to an emergency department.
Objective documentation of the pathology on temporal artery biopsy or specific arterial imaging can help avoid unnecessary long-term systemic corticosteroid treatment and its potential adverse effects.
Temporal artery biopsy historically has been considered the gold-standard investigation to diagnose giant cell arteritis. The advent of newer imaging techniques may have reduced the need for temporal artery biopsy in some centres. Specific imaging may not be available beyond metropolitan centres.
Although temporal artery biopsy should be performed promptly, do not delay treatment if giant cell arteritis is suspected. Pathological arterial changes persist for at least 2 to 4 weeks after treatment has been started. Starting treatment does not impair the diagnostic accuracy of temporal artery biopsy within 1 week; it may still be useful at 2 to 4 weeks.
When a temporal artery biopsy is performed it is imperative to obtain an adequate sample (at least 2 cm of the artery) and to have the sample comprehensively assessed. Multiple sections of the artery should be examined, because giant cell arteritis may present with ‘skip’ lesions1. There is no benefit in performing a contralateral biopsy if the initial biopsy was of adequate length and comprehensively assessed as having no evidence of arteritis; the result is unlikely to be different.
Specialised vascular imaging including ultrasound and magnetic resonance imaging (MRI) scans are accepted noninvasive diagnostic tools for giant cell arteritis. The most specific ultrasound finding is a noncompressible ‘halo’ sign in the cranial arteries. The most specific sign on high-resolution MRI scan is mural inflammation of the cranial arteriesDejaco, 2018.
Positron emission tomography (PET) scan or computed tomography angiography (CTA) may also be useful. MRI, PET and CTA scans can all image the aorta and its major branches to identify predominantly large-vessel disease in patients without temporal artery involvement (which occurs in approximately 20% of cases)Dejaco, 2018.
Expert competency in, and access to, specialised vascular imaging (beyond metropolitan hospitals) may limit their utility within Australia for the diagnosis of giant cell arteritis. In rural and remote areas, temporal artery biopsy remains the investigation of first choice.
When there is a high clinical suspicion (ie high pretest probability) of giant cell arteritis, a negative result on temporal artery biopsy or specific imaging does not exclude the diagnosis. A second investigation should be considered if the first is negative.