A new headache and a difficult decision

Three weeks of new persistent right temporal headache, about 6/10, sometimes waking her. Brushing her hair hurts. No preceding head injury, abrupt thunderclap onset, fever with neck stiffness, or new focal weakness or speech disturbance.

For five days, her jaw has ached after two to three minutes of sustained chewing. Resting for one to two minutes relieves it. Clarify this pattern rather than recording only ‘jaw pain’. She has no usual clicking or focal dental pain. Symptoms can overlap: the pattern supports claudication but is not independently diagnostic.

Two painless episodes during the last 48 hours: a grey curtain obscured the whole right eye for three to four minutes, then for about two minutes. She checked each eye separately during an episode. Vision recovered to her usual baseline. No current visual loss, double vision, red painful eye or flashing zigzags.

Roleplayer: do not conceal this after a clear question about any change in sight. If the candidate identifies it, permit immediate escalation while the remaining history continues. A teaching timer must never imply that a real emergency should wait until the consultation ends.

Six weeks of shoulder and hip-girdle aching with more than an hour of morning stiffness. Dressing and rising are painful; she does not describe loss of muscle power. Fatigue, reduced appetite and about 3 kg unintentional weight loss over two months. No arm claudication or new chest/back pain.

Ask how illness affects eating, sleep and care of her husband. These establish both disease burden and whether the proposed treatment plan is practicable.

Hypertension, diet-controlled type 2 diabetes, osteopenia on DXA two years ago, previous bilateral cataract surgery and past shingles. Amlodipine 5 mg daily, atorvastatin 20 mg at night, colecalciferol 800 units daily and paracetamol up to 1 g four times daily for this headache. No current glucocorticoid or anticoagulant. Penicillin previously caused a rash without anaphylaxis.

Former smoker, approximately 15 pack-years; little alcohol. Ask about recent infection, prior steroid effects and fracture history before planning preventive care, without postponing emergency treatment.

Her husband Gerald, 78, has moderate Alzheimer disease. Carers attend twice daily for personal care, but he cannot safely be left alone overnight. Daughter Fiona lives about three hours away. Margaret proposes going home and returning next week.

Her mother developed bruising while taking steroids. Margaret worries about diabetes and weakened bones. Roleplayer: acknowledge a concrete plan for Gerald, but do not agree merely because the candidate repeatedly says ‘urgent’. A respectful explanation may still lead to questions or refusal; the aim is an informed decision, not compliance at any cost.

Alert and comfortable. Pulse 82/min, BP 148/84 mmHg, respiratory rate 16/min, oxygen saturation 97% on air, temperature 37.2°C. Capillary glucose 6.4 mmol/L. Weight 58 kg, height 1.61 m. Normal observations do not measure the risk to her sight.

Explain and obtain consent before touching the painful scalp. Compare both temporal arteries: the right is thickened, tender and beaded with reduced pulsation; the left is unremarkable. Examine the jaw and relevant cranial nerves as indicated.

Measure distance acuity in each eye with appropriate distance correction: 6/9 bilaterally, her baseline. Pupils show no relative afferent defect; confrontation fields, eye movements and fundoscopy are unremarkable. State the limits of a bedside examination. These findings do not exclude intermittent ischaemia, GCA or other ocular disease, and do not prove that no injury has occurred. Do not invent disc swelling to make the diagnosis easier.

BP in the left arm is 146/82 mmHg. Peripheral pulses are symmetric and there are no audible subclavian bruits. Active shoulder abduction is painful at about 80 degrees, with preserved passive range and normal power when pain is accommodated. No focal neurological deficit.

Girdle findings support a polymyalgic syndrome rather than proven primary muscle weakness. Normal pulses and similar arm pressures do not exclude silent large-vessel involvement. A specialist decides whether vascular imaging is appropriate; a normal bedside examination is not a blanket reason to omit it.

Obtain ESR/CRP and FBC before, or promptly after, the first steroid dose if sampling would delay treatment. Supplied results: ESR 78 mm/hour, CRP 96 mg/L, haemoglobin 108 g/L, MCV 88 fL and platelets 486 × 10⁹/L. The inflammatory pattern supports the clinical suspicion but does not establish the diagnosis alone.

Renal profile: sodium 137, potassium 4.3 mmol/L, creatinine 76 micromol/L. Albumin 32 g/L, ALP 160 U/L, ALT 26 U/L. HbA1c 47 mmol/mol. These inform baseline health and treatment monitoring; mild ALP elevation is not proof of a separate hepatobiliary diagnosis. Investigate other abnormalities according to the clinical context.

Arrange prompt specialist vascular ultrasound of temporal and axillary arteries and/or temporal artery biopsy through the local pathway. BSR recommends a biopsy specimen at least 1 cm long; timing, technique and interpretation matter. Explain that neither test is perfect.

A scan after several days of steroids may have reduced sensitivity. A negative result requires reconsideration of the original probability, test quality and alternatives, not automatic treatment cessation. If probability remains high, rheumatology may arrange biopsy or further imaging. Do not teach steroid response as a specific diagnostic test.

My leading diagnosis is suspected giant cell arteritis with transient monocular visual loss and associated polymyalgic symptoms. The combination of new headache, jaw claudication, temporal artery abnormality and inflammation is compelling. Sight has recovered, but the risk is time-critical.

Embolic retinal ischaemia is an important competing or coexisting cause of the visual episodes; vascular risk assessment and specialist investigation may be needed in parallel. Raised inflammatory markers do not exclude embolism. Migraine, temporomandibular disease and angle-closure glaucoma fit less well here, but should be judged from the complete history and examination, not excluded by a single negative feature.

Interrupt routine assessment to contact the senior acute clinician and ophthalmology for same-day assessment, with rheumatology involvement. Start glucocorticoid treatment immediately when GCA is strongly suspected; neither blood results nor imaging should postpone it.

For acute or intermittent visual loss, BSR conditionally supports intravenous methylprednisolone 500 mg–1 g daily for up to three days, followed by oral treatment. Arrange this with the treating specialist under the local emergency pathway. If IV treatment is not immediately available, do not leave the patient untreated while it is organised: BSR describes oral prednisolone 60–100 mg daily for up to three days when IV treatment is not possible. The responsible clinician selects the regimen, checks prescribing risks and records the first dose and time.

This visual presentation is not a routine low-dose PMR pathway. A general fast-track appointment several working days away is not an adequate response to her visual history. Existing visual loss would still require urgent assessment; never tell a patient that treatment is now pointless or that sight recovery is impossible in an individual case.

‘I am concerned about inflammation in the arteries, called giant cell arteritis. The headache and jaw symptoms support this, and the brief loss of sight could mean the blood supply to your eye was affected. Other causes are possible, but waiting risks permanent harm to sight. I recommend treatment and an eye specialist today, while we organise tests to confirm the cause.’

‘I cannot promise that treatment removes every risk, but it is important to begin promptly. Your worries about sugar levels and bones are real. We will monitor your glucose and arrange protection and follow-up alongside treatment, rather than ignore those problems.’ Pause for questions. Ask her to explain what makes today different from an ordinary headache appointment.

Ask permission to contact Fiona and establish who is with Gerald now. Involve the care agency and hospital discharge/social-care team to arrange emergency cover. Confirm an actual person and time rather than promising that a social worker will definitely arrive within an hour. Begin this work while treatment is being arranged.

If she still wants to leave, explore the reason and her understanding of the risks, assess decision-specific capacity where in doubt and obtain senior help. Do not equate disagreement with incapacity. Document an informed refusal, the practical support offered, immediate safety advice and a route back to care. Do not simply book a review next week.

Rheumatology will guide oral treatment and tapering after disease control, considering symptoms, inflammatory markers and adverse effects. Do not give an automatic taper detached from review. Arrange glucose monitoring and a plan for hyperglycaemia, blood-pressure checks, fracture-risk assessment and bone protection. Assess the need for gastric protection rather than assuming every adjunct is mandatory.

Explain the steroid emergency card and why prolonged treatment must not be stopped abruptly. Give a contact for infection concerns and significant exposure to chickenpox or shingles. New or recurrent visual disturbance needs immediate emergency eye assessment, even if transient. Recurrent jaw pain or headache after improvement requires urgent specialist contact. Provide named follow-up and written instructions; do not rely on ‘come back if worse’.

Escalate immediately to the emergency ophthalmology/acute team and continue the urgent treatment pathway. Document timing and current acuity without delaying care. Do not promise recovery or assume nothing can be done; protecting remaining vision and specialist assessment remain essential.

This weakens one supporting element but does not negate a convincing ischaemic history. Reassess alternative causes promptly and discuss with specialists; normal markers alone must not cancel urgent assessment or treatment when GCA remains strongly suspected.

Possible relapse with ischaemic symptoms: urgent specialist reassessment of treatment, adherence and alternatives. Do not wait for the next routine visit or self-adjust to a preprinted taper. Any accompanying visual change requires immediate eye assessment.

Activate the emergency stroke pathway alongside the GCA assessment. Do not attribute every new neurological symptom to known vasculitis without urgent evaluation. Communicate treatment already given and symptom onset accurately.

Strong: Clarifies monocular loss, recovery and chewing-related symptoms, and keeps retinal embolism in the differential.

Incomplete: Labels visual symptoms ‘blur’ without establishing their character.

Unsafe: Reassures because sight returned or calls the presentation simple PMR.

Strong: Documents actual acuity, pupils, discs and temporal findings, with their limitations.

Incomplete: Says ‘eyes normal’ without describing assessment.

Unsafe: Invents an afferent defect or delays emergency treatment to finish an exhaustive examination.

Strong: Starts the urgent treatment pathway and same-day ophthalmology while arranging confirmation.

Incomplete: Says ‘refer’ without urgency or responsibility.

Unsafe: Waits for ultrasound or sends her home untreated for routine review.

Strong: Balances sight risk and steroid harms, checks understanding and confirms care for Gerald.

Incomplete: Acknowledges the caring role without practical action.

Unsafe: Coerces consent, dismisses harms or assumes refusal means incapacity.

Transient visual loss is not reassuring simply because sight has returned. In this presentation it is the feature that makes assessment and treatment immediately time-critical.

A normal current eye examination documents the present state; it does not exclude intermittent retinal ischaemia or GCA.

When GCA is strongly suspected, treatment and diagnostic confirmation proceed in parallel. Do not wait for inflammatory markers, ultrasound or biopsy before protecting vision.

A negative ultrasound is interpreted with the original clinical probability, test quality and time after glucocorticoids; it is not an automatic instruction to stop treatment.

PACES-level performance includes solving the practical barrier to care, here the patient's responsibility for her husband, while respecting capacity and avoiding coercion.

Rehearse a 90-second explanation that names the suspected diagnosis, explains why transient visual loss is urgent, acknowledges steroid harms, states the immediate plan and checks understanding. Repeat with the variation that the patient still wishes to leave.