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Stem
A 72-year-old woman presents to the emergency department with a three-week history of new left-sided temporal headache, scalp tenderness when she brushes her hair, and pain in her jaw that comes on after a few minutes of chewing and eases with rest. This morning she noticed transient blurring of vision in the left eye lasting ten minutes that has now resolved. She has felt generally unwell with night sweats and has lost three kilograms. She also describes bilateral shoulder and hip stiffness for two months, worse in the morning. Blood pressure is 150/85 mmHg in the right arm and 142/80 in the left. Temperature 37.6 °C. Temporal arteries are tender and thickened with reduced pulse on the left.
Questions
a) What is the most likely diagnosis and what two features make this a clinical emergency? (2 marks)
b) Outline the focused examination and immediate investigations. (3 marks)
c) Detail your immediate and subsequent management with drug doses. (3 marks)
d) List the complications and the long-term follow-up required. (2 marks)
Model answers
a) The diagnosis is giant cell arteritis with threatened vision (amaurosis fugax) and coexistent polymyalgia rheumatica (new temporal headache, scalp tenderness, jaw claudication, tender thickened temporal artery, raised inflammatory markers expected, PMR symptoms).
The two emergency features are:
- Transient visual loss (amaurosis fugax) — impending permanent anterior ischaemic optic neuropathy; the second eye can be lost within days.
- The risk of irreversible blindness if glucocorticoids are delayed — treatment must begin before any investigation.
b) Examination: visual acuity and fields, fundoscopy (pale swollen disc in AION), extraocular movements, both arm blood pressures, palpation of temporal arteries (tenderness, thickening, reduced pulse), peripheral pulses and bruits (subclavian, axillary, carotid, abdominal aorta), cardiac auscultation (aortic regurgitation), and shoulder/pelvic-girdle ROM for PMR.
Investigations (do not delay treatment): ESR and CRP (expected over 50 mm/h; CRP more sensitive), FBC (normocytic anaemia, thrombocytosis), UEC, LFT, glucose, CK. Temporal artery biopsy within 2 weeks of starting steroids (skip lesions give 10 to 15 percent false negatives). Colour duplex ultrasound (halo sign) or PET-CT/MRA if large-vessel disease is suspected.
c) Immediate: IV methylprednisolone 500 mg to 1 g once daily for 3 days (because of amaurosis fugax), without waiting for biopsy or any test. Then oral prednisolone 1 mg/kg (typically 60 mg) daily.
Subsequent: temporal artery biopsy within 2 weeks. Taper prednisolone slowly over 12 to 24 months once symptoms and CRP are controlled (10 mg every 2 weeks to 20 mg, then 2.5 mg every 2 to 4 weeks to 10 mg, then 1 mg every 4 weeks). Add tocilizumab 162 mg subcutaneously weekly for steroid-sparing (GiACTA trial) at induction if steroid toxicity is likely or on relapse. Bone protection (calcium 1000 mg and vitamin D 800 to 1000 IU daily, bisphosphonate such as alendronate 70 mg weekly, DEXA), PPI (omeprazole 20 mg), and low-dose aspirin 75 mg daily.
d) Disease complications: permanent blindness (anterior ischaemic optic neuropathy), posterior-circulation stroke, thoracic aortic aneurysm and dissection (excess late mortality), limb claudication, scalp or tongue necrosis. Treatment complications: osteoporotic fracture, diabetes, hypertension, infection, adrenal suppression, cataract from long-term steroids; infection and transaminitis from tocilizumab.
Long-term follow-up: clinical and ESR/CRP review every 4 to 8 weeks during taper; steroid-toxicity surveillance (DEXA, glucose, lipids, intra-ocular pressure); annual aortic imaging (CT or MR angiography) for life in large-vessel GCA; lifelong counselling to report visual symptoms immediately.