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EMERGENCY

Giant Cell Arteritis (Temporal Arteritis)

High EvidenceUpdated: 2025-12-23

On This Page

Red Flags

  • Visual symptoms (transient or permanent) — AION, CRAO
  • Jaw claudication (highly specific)
  • Scalp tenderness or necrosis
  • Sudden blindness
  • Diplopia
  • Stroke symptoms in older patient
Overview

Giant Cell Arteritis (Temporal Arteritis)

1. Clinical Overview

Summary

Giant Cell Arteritis (GCA) is a systemic large and medium vessel vasculitis that predominantly affects the cranial branches of the aorta, particularly the temporal arteries. It is a medical emergency because untreated GCA causes permanent visual loss in 15-20% of patients. GCA almost exclusively affects individuals over 50 years (peak age 70-80) and is strongly associated with polymyalgia rheumatica (PMR). The classic presentation is new-onset headache, scalp tenderness, jaw claudication, and markedly elevated inflammatory markers (ESR greater than 50, often greater than 100). Immediate high-dose glucocorticoids (prednisolone 60mg or IV methylprednisolone if visual symptoms) must be started on clinical suspicion — do NOT wait for biopsy confirmation. Temporal artery biopsy remains the gold standard for diagnosis, though ultrasound (halo sign) is increasingly used. Tocilizumab is now used as a steroid-sparing agent for relapsing or refractory disease.

Key Facts

  • Definition: Large/medium vessel granulomatous vasculitis affecting aortic branches, predominantly cranial arteries
  • Age: Greater than 50 years (by definition); peak 70-80 years
  • Sex: Female:Male 2-3:1
  • Emergency: 15-20% risk of permanent blindness if untreated
  • Key symptom: New-onset headache + scalp tenderness in patient greater than 50
  • Specific sign: Jaw claudication (pain on chewing — 90% specificity)
  • Inflammatory markers: ESR greater than 50 (often greater than 100), CRP elevated
  • Treatment: Immediate high-dose prednisolone (60mg) or IV methylprednisolone if visual symptoms

Clinical Pearls

"Don't Wait for the Biopsy": If GCA is clinically suspected, START STEROIDS IMMEDIATELY. Biopsy remains positive for up to 2 weeks after steroids are started. Delay risks permanent blindness.

Jaw Claudication is Gold: Jaw claudication (pain in the jaw muscles when chewing that is relieved by rest) is approximately 90% specific for GCA. It is caused by ischaemia of the masseter muscles.

The PMR-GCA Spectrum: 50% of GCA patients have symptoms of PMR. 10-20% of PMR patients will develop GCA. Always ask about headache and visual symptoms in PMR.

Why This Matters Clinically

GCA is a true emergency. Once vision is lost, it rarely recovers. The key is high clinical suspicion in any patient over 50 with new headache, temporal symptoms, or unexplained raised inflammatory markers. Starting steroids immediately can prevent blindness.


2. Epidemiology

Incidence & Prevalence

  • Incidence: 15-25 per 100,000 in those greater than 50 years (higher in Northern Europe)
  • Peak age: 70-80 years
  • Lifetime risk: Approximately 1% for women, 0.5% for men
  • Geographic variation: Higher in Scandinavian and Northern European populations

Demographics

FactorDetails
AgeAlways greater than 50 years (typically 70-80)
SexFemale:Male 2-3:1
EthnicityMost common in Caucasians; rare in Asian and African populations
GeographyHigher in Northern Europe, North America

Risk Factors

Non-Modifiable:

  • Age greater than 50 years
  • Female sex
  • Northern European ancestry
  • Family history
  • HLA-DR4 association

Modifiable:

Risk FactorAssociation
SmokingPossible association
Prior PMR10-20% develop GCA
InfectionsPossible trigger (varicella zoster, parvovirus)

3. Pathophysiology

Mechanism

Step 1: Trigger (Possibly Infectious/Environmental)

  • Unknown trigger activates dendritic cells in adventitia of large vessels
  • Possible infectious triggers include varicella zoster virus

Step 2: T-Cell Mediated Immune Response

  • Activated dendritic cells present antigens to CD4+ T-helper cells
  • Th1 and Th17 cells release IFN-γ, IL-17, and other inflammatory cytokines
  • Macrophages recruited and fuse to form multinucleated giant cells

Step 3: Granulomatous Inflammation

  • Transmural inflammation centred on internal elastic lamina
  • Giant cells (fused macrophages) attack elastic tissue
  • Intimal proliferation causes luminal narrowing

Step 4: Ischaemic Complications

  • Luminal stenosis or occlusion of affected arteries
  • Temporal artery involvement: headache, scalp tenderness
  • Ophthalmic artery: anterior ischaemic optic neuropathy (AION), central retinal artery occlusion (CRAO)
  • Large vessel involvement: aortic aneurysm, limb claudication, stroke

Classification

TypeFeatures
Cranial GCAClassic presentation with headache, temporal artery involvement, visual symptoms
Large Vessel GCAAorta and major branches involved; may present without headache
Occult GCARaised inflammatory markers, constitutional symptoms, no classic cranial features

Association with PMR

ConditionOverlap
GCA with PMR40-50% of GCA patients have PMR symptoms
PMR progressing to GCA10-20% of PMR patients develop GCA
Clinical significanceAlways screen PMR patients for headache, jaw claudication, visual symptoms

4. Clinical Presentation

Symptoms

Classic Presentation:

Visual Symptoms (EMERGENCY):

PMR Symptoms (if present):

Signs

General:

Head and Neck:

Eyes:

Red Flags

[!CAUTION] Red Flags — IMMEDIATE steroids required if:

  • ANY visual symptoms (transient or permanent)
  • Jaw claudication (highly specific for GCA)
  • Temporal artery tenderness or reduced pulsation
  • New headache in patient greater than 50 with raised ESR/CRP
  • Diplopia
  • Scalp necrosis (rare, late sign)

New-onset headache (70-90%) — Often temporal, described as constant, boring, or throbbing
Common presentation.
Scalp tenderness (60%) — Pain when combing hair or lying on pillow
Common presentation.
Jaw claudication (40-50%) — Pain in jaw muscles when chewing; highly specific (90%)
Common presentation.
Constitutional symptoms (50%) — Fatigue, malaise, weight loss, low-grade fever
Common presentation.
5. Clinical Examination

Structured Approach

General:

  • Vital signs (low-grade fever possible)
  • Assess for weight loss, malaise

Head and Neck:

  • Inspect temporal arteries (both sides): visible swelling?
  • Palpate: tenderness, thickening, reduced or absent pulsation
  • Scalp tenderness
  • Jaw claudication (ask to chew repeatedly)

Eyes:

  • Visual acuity
  • Pupillary reflexes (RAPD)
  • Fundoscopy (pale swollen disc in AION)
  • Eye movements (diplopia/restriction)

Musculoskeletal:

  • Shoulder and hip range of motion (PMR assessment)
  • Proximal muscle tenderness

Special Tests

TestTechniquePositive FindingClinical Significance
Temporal artery palpationPalpate along course of STATender, thickened, non-pulsatileGCA likely
RAPD (swinging flashlight test)Shine light from one eye to otherPupil dilates on affected sideOptic nerve ischaemia
Jaw claudication testAsk patient to chew for 1-2 minutesPain develops, relieved by rest90% specific for GCA
PMR screenAssess shoulder/hip ROM and stiffnessRestricted, painfulAssociated PMR

6. Investigations

First-Line (Urgent)

  • ESR — Typically greater than 50; often greater than 100
  • CRP — Elevated (correlates well with activity)
  • FBC — Normocytic anaemia, thrombocytosis common
  • LFTs — Raised ALP (30%)

Laboratory Tests

TestExpected FindingPurpose
ESRGreater than 50 (often greater than 100)Key diagnostic marker
CRPElevatedMore sensitive; rises and falls faster than ESR
FBCNormocytic anaemia; thrombocytosisChronic inflammation
LFTsRaised ALPHepatic involvement in systemic inflammation
U&EsUsually normalBaseline before steroids
GlucoseBaselineMonitor during steroids

Imaging

ModalityFindingsIndication
Ultrasound temporal artery"Halo sign" — hypoechoic wall thickeningFirst-line; rapid, non-invasive
Temporal artery biopsyGranulomatous inflammation, giant cells, intimal proliferationGold standard; arrange within 2 weeks
CTA/MRALarge vessel involvement (aorta, subclavian)Suspected large vessel GCA
PET-CTVascular FDG uptakeActive large vessel vasculitis

Temporal Artery Biopsy

Technique:

  • Minimum 2 cm segment (skip lesions common)
  • Positive result confirms diagnosis
  • Negative does not exclude — sensitivity 50-80%
  • Can remain positive up to 2 weeks after steroids started

Histology:

  • Granulomatous inflammation centred on internal elastic lamina
  • Multinucleated giant cells
  • Intimal proliferation
  • Fragmentation of internal elastic lamina

Diagnostic Criteria

1990 ACR Classification Criteria (≥3 of 5):

  1. Age at onset ≥50 years
  2. New headache
  3. Temporal artery abnormality (tenderness, reduced pulse)
  4. ESR ≥50
  5. Abnormal temporal artery biopsy

Sensitivity 93%, Specificity 91%


7. Management

Management Algorithm

Immediate Management (Emergency)

HIGH Clinical Suspicion — Don't Wait for Biopsy:

PresentationTreatment
GCA without visual symptomsPrednisolone 40-60mg PO daily
GCA WITH visual symptomsIV Methylprednisolone 1g daily × 3 days → then oral prednisolone 60mg
Recent or evolving visual lossUrgent ophthalmology + IV steroids

Long-Term Steroid Therapy

Taper Schedule (Example — BSR Guideline):

  • Prednisolone 40-60mg daily for 2-4 weeks (until symptoms resolve and markers normalise)
  • Reduce by 10mg every 2 weeks until 20mg
  • Reduce by 2.5mg every 2-4 weeks until 10mg
  • Reduce by 1mg every 1-2 months thereafter
  • Total duration: 1-2 years minimum (often longer)

Monitoring:

  • ESR/CRP monthly initially, then less frequently
  • Symptoms of relapse (headache, jaw claudication, visual symptoms, PMR symptoms)
  • Steroid side effects (glucose, BP, bone health)

Adjunctive Therapy

DrugDosePurpose
Low-dose aspirin75mg dailyReduces ischaemic events (BSR recommends)
BisphosphonateAlendronate 70mg weeklyBone protection (long-term steroids)
Calcium + Vitamin D1000mg Ca / 800IU D3 dailyBone protection
PPIOmeprazole 20mgGI protection (especially if on aspirin)

Steroid-Sparing Agents

DrugDoseIndication
Tocilizumab162mg SC weekly OR 8mg/kg IV monthlyRelapsing/refractory GCA; reduces steroid burden; NICE approved
Methotrexate15-25mg weeklyAlternative; less evidence than tocilizumab

Disposition

  • Urgent ophthalmology referral: Any visual symptoms
  • Rheumatology referral: All patients for ongoing management
  • Vascular surgery/radiology: If large vessel GCA suspected (aortic imaging)
  • Follow-up: Initially 2-weekly, then monthly; taper over 1-2+ years

8. Complications

Immediate (Hours-Days)

ComplicationIncidencePresentationManagement
Permanent visual loss15-20% if untreatedSudden painless monocular vision lossImmediate IV methylprednisolone
Stroke2-4%Sudden neurological deficitAcute stroke management

Early (Weeks-Months)

  • Disease relapse: Return of symptoms during taper; requires steroid dose increase
  • Steroid side effects: Hyperglycaemia, hypertension, weight gain, mood changes, insomnia
  • Second eye involvement: 25-50% risk if first eye affected and untreated

Late (Years)

  • Aortic aneurysm: 10-20% of GCA patients; aortic aneurysm/dissection risk elevated
  • Osteoporosis: From prolonged steroid therapy
  • Cataracts, glaucoma: Steroid complications
  • Diabetes mellitus: Steroid-induced
  • Adrenal suppression: From prolonged steroids; taper slowly

9. Prognosis & Outcomes

Natural History

  • Untreated: High risk of permanent bilateral blindness (15-20%)
  • With steroids: Excellent symptom control; majority achieve remission
  • Average treatment duration: 1-2 years; some require longer

Outcomes with Treatment

VariableOutcome
Remission with steroids90%+
Relapse during taper40-50%
Permanent visual loss (treated)Less than 5% if treated early
Duration of treatmentMedian 2 years
Long-term aortic complications10-20%

Prognostic Factors

Good Prognosis:

  • Rapid diagnosis and treatment
  • No visual symptoms at presentation
  • Good response to steroids
  • Tocilizumab use in relapsing disease

Poor Prognosis:

  • Visual symptoms at presentation
  • Delayed treatment
  • Large vessel involvement
  • Frequent relapses
  • Steroid intolerance

10. Evidence & Guidelines

Key Guidelines

  1. BSR/BHPR Guideline (2020) — Management of Giant Cell Arteritis. Recommends immediate steroids, aspirin, tocilizumab for relapse. BSR
  2. EULAR Recommendations (2018) — Imaging in large vessel vasculitis. Supports ultrasound as first-line. EULAR
  3. ACR 1990 Classification Criteria — Standard diagnostic criteria. ACR

Landmark Trials

GiACTA Trial (Stone et al. 2017) — Tocilizumab for GCA

  • 251 patients randomised to tocilizumab vs placebo
  • Key finding: Tocilizumab + short steroid taper superior to steroids alone for sustained remission (56% vs 14%)
  • Clinical Impact: Tocilizumab now first-line steroid-sparing agent

Proven et al. (2002) — Visual outcomes in GCA

  • Retrospective cohort
  • Key finding: 25-50% of untreated patients with unilateral visual loss develop bilateral blindness
  • Clinical Impact: Emphasises urgency of treatment

TABUL Study (Luqmani et al. 2016) — Ultrasound in GCA

  • Pragmatic trial comparing ultrasound to biopsy
  • Key finding: Ultrasound "halo sign" has 77% sensitivity, 96% specificity
  • Clinical Impact: Supports ultrasound as first-line imaging modality

Evidence Strength

InterventionLevelKey Evidence
Immediate high-dose steroids4Expert consensus; ethical barrier to RCT
IV methylprednisolone for visual symptoms4Expert consensus
Tocilizumab1bGiACTA RCT
Ultrasound "halo sign"2aTABUL study
Low-dose aspirin2aObservational studies

11. Patient/Layperson Explanation

What is Giant Cell Arteritis?

Giant Cell Arteritis (GCA), also called Temporal Arteritis, is an inflammation of the blood vessels, especially the arteries in your temples (the sides of your head). It mainly affects people over 50. The inflammation can reduce blood flow through these arteries, which can cause serious problems — including permanent blindness if not treated quickly.

Is it serious?

Yes, GCA is a medical emergency because of the risk to your vision. Without treatment, about 1 in 5 people with GCA will lose some or all of their sight. The good news is that treatment with steroids is very effective if started early — this is why doctors will often start treatment immediately if they suspect GCA, even before confirming the diagnosis with tests.

How is it treated?

  1. Steroids (prednisolone): High-dose steroid tablets are started immediately. If you have any problems with your vision, you may be given steroids through a drip first.
  2. Long-term treatment: You will need to take steroids for 1-2 years, gradually reducing the dose. This is to keep the inflammation under control and prevent it coming back.
  3. Bone protection: Because steroids can weaken bones over time, you will likely be given tablets to protect your bones.
  4. Aspirin: A low dose of aspirin is often recommended to help prevent blockages in the blood vessels.
  5. Newer treatments: A medication called tocilizumab can be used if the condition keeps coming back or if steroids are causing too many side effects.

What to expect

  • Symptoms usually improve within days of starting steroids
  • Blood tests (ESR and CRP) are used to monitor your condition
  • You'll be followed up regularly and the steroid dose will be slowly reduced
  • Relapses can happen, especially when reducing the dose — this is why tapering is done very slowly

When to seek help

See a doctor immediately (this is an emergency) if:

  • You notice any change in your vision (blurred, double, or partial loss)
  • You develop a new headache, especially if you're over 50
  • You have pain in your jaw when chewing
  • Your scalp feels tender
  • You feel generally unwell with high inflammatory markers

12. References

Primary Guidelines

  1. Mackie SL, et al. British Society for Rheumatology guideline on diagnosis and treatment of giant cell arteritis. Rheumatology (Oxford). 2020;59(3):e1-e23. PMID: 31970405
  2. Dejaco C, et al. EULAR recommendations for the use of imaging in large vessel vasculitis in clinical practice. Ann Rheum Dis. 2018;77(5):636-643. PMID: 29358285

Key Trials

  1. Stone JH, et al. Trial of Tocilizumab in Giant-Cell Arteritis (GiACTA). N Engl J Med. 2017;377(4):317-328. PMID: 28745999
  2. Luqmani R, et al. The Role of Ultrasound Compared to Biopsy of Temporal Arteries in the Diagnosis and Treatment of Giant Cell Arteritis (TABUL). Ann Rheum Dis. 2016;75(6):996-1002. PMID: 26888949
  3. Proven A, et al. Glucocorticoid therapy in giant cell arteritis: duration and adverse outcomes. Arthritis Rheum. 2003;49(5):703-708. PMID: 14558057

Further Resources

  • Versus Arthritis GCA: versusarthritis.org/about-arthritis/conditions/giant-cell-arteritis
  • NHS Giant Cell Arteritis: nhs.uk/conditions/temporal-arteritis
  • RNIB (sight loss support): rnib.org.uk


Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Giant Cell Arteritis is a medical emergency. If you suspect GCA or have any visual symptoms, seek immediate medical attention.

Last updated: 2025-12-23

At a Glance

EvidenceHigh
Last Updated2025-12-23
Emergency Protocol

Red Flags

  • Visual symptoms (transient or permanent) — AION, CRAO
  • Jaw claudication (highly specific)
  • Scalp tenderness or necrosis
  • Sudden blindness
  • Diplopia
  • Stroke symptoms in older patient

Clinical Pearls

  • **"Don't Wait for the Biopsy"**: If GCA is clinically suspected, START STEROIDS IMMEDIATELY. Biopsy remains positive for up to 2 weeks after steroids are started. Delay risks permanent blindness.
  • **The PMR-GCA Spectrum**: 50% of GCA patients have symptoms of PMR. 10-20% of PMR patients will develop GCA. Always ask about headache and visual symptoms in PMR.
  • **Red Flags — IMMEDIATE steroids required if:**
  • - ANY visual symptoms (transient or permanent)
  • - Jaw claudication (highly specific for GCA)

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines