Diagnosis
Giant cell arteritis (temporal arteritis)
Key clinical clues
- New headache over age 50 with scalp tenderness in a new distribution
- Jaw claudication, pain on chewing that resolves with rest, the most specific symptom
- Thickened, tender, pulseless temporal artery with a normal contralateral vessel
- ESR 96 with thrombocytosis and normocytic anemia; normal CK despite girdle stiffness
- Transient monocular visual loss, do not wait for biopsy before starting steroids
First-line treatment
Immediate high-dose glucocorticoids
New-onset headache over 50 with scalp tenderness and a markedly raised ESR is giant cell arteritis until disproven, and the jaw claudication settles it: pain that comes on with chewing and resolves with rest is the single most specific symptom, reflecting ischemia of the masseter through branches of the external carotid. The pulseless temporal artery on one side with a normal vessel opposite is the characteristic finding, and the girdle stiffness is the polymyalgia rheumatica that coexists in roughly half of cases; a normal creatine kinase distinguishes this from an inflammatory myopathy, and the raised alkaline phosphatase is the mild cholestatic picture of active disease, not liver or bone pathology. The episode of transient monocular visual loss is amaurosis fugax from involvement of the posterior ciliary arteries, and untreated it heralds permanent, painless and irreversible blindness, which can arrive within days and may then take the second eye. Ultrasound showing a non-compressible halo supports the diagnosis, and the thickened right axillary artery marks this as a large-vessel vasculitis reaching well beyond the temple. Biopsy is confirmatory, but the critical management principle is that high-dose glucocorticoids must be started the moment the diagnosis is suspected, without waiting for either. Because she has already had amaurosis fugax, that means intravenous methylprednisolone rather than the oral prednisolone which would serve for headache alone. Biopsy stays informative for about two weeks after steroids begin, and the skip lesions here explain why specimen length matters and why a negative biopsy does not exclude the disease. Tocilizumab is added as a steroid-sparing agent given the long treatment course and the burden of steroid toxicity in this age group, with bone and gastric protection alongside it for the same reason.