Changes

January 2026 — reviewed. A literature search was conducted in November 2025 to identify evidence-based guidelines, UK policy, systematic reviews, and key randomized controlled trials published since the last revision of this topic. No major changes to recommendations have been made. An Assessment node has been added to the Diagnosis section in line with current CKS style. The section on Prescribing information has been removed and a link provided to the CKS topic on Corticosteroids - oral.

Update

Goals

To support primary healthcare professionals to:

• Identify suspected giant cell arteritis.
• Refer urgently to a specialist for further assessment and treatment to minimize the risk of complications, such as permanent vision loss.
• Ensure appropriate monitoring and management are provided following specialist assessment.
• Recognize a relapse of symptoms and complications of GCA and manage appropriately.
• Advise the person about sources of information and support.
• Minimize the risks of long-term glucocorticoid treatment.

Outcome measures

Audit criteria

QOF indicators

QIPP - Options for local implementation

NICE quality standards

Headaches in over 12s

• People diagnosed with a primary headache disorder have their headache type classified as part of the diagnosis.

[NICE, 2013]

What is it?

• Giant cell arteritis (GCA) is a chronic vasculitis characterized by granulomatous inflammation in the walls of medium and large arteries, with associated concentric intimal hyperplasia [Mackie, 2020a]. A person may have vasculitis limited to the cranial arteries, additional extra-cranial involvement, or isolated extra-cranial involvement [Bosch, 2024].
  • Cranial GCA, also known as 'temporal arteritis', occurs when the extracranial branches of the carotid artery, such as the temporal artery, facial, maxillary, and/or occipital artery and their branches, along with branches of the ophthalmic artery, responsible for ocular perfusion, are potentially involved [Bosch, 2024].
  • Extra-cranial or large vessel GCA typically causes inflammation of the thoracic aorta and/or its proximal secondary or tertiary branches, but may also affect the external carotid, internal carotid, and vertebral arteries [Riambau, 2017; Mackie, 2020a; Bosch, 2024].
• A relapse of GCA is defined as the recurrence of symptoms or signs of active disease, ischaemic complications, or symptoms of polymyalgia rheumatica not attributable to another underlying cause, with or without changes in blood inflammatory markers (erythrocyte sedimentation rate and/or C-reactive protein) during glucocorticoid tapering or glucocorticoid-free treatment phases [Mackie, 2020a; Hellmich, 2020; Bosch, 2024]. See the CKS topic on Polymyalgia rheumatica for more information.
• Refractory GCA is defined as a disease where there is an inability to achieve remission despite 'standard care' treatment with a course of glucocorticoids, which would be considered adequate to induce remission [Lyons, 2020; Bosch, 2024].

What causes it?

The exact cause of giant cell arteritis (GCA) is unknown, but it is likely to be an immune-mediated vasculitis [Riambau, 2017] [van der Geest, 2024].

• There is typical involvement of the arteries arising from the cranial branches of the aortic arch, and the extracranial branches of the carotid arteries [Lazarewicz, 2019].
• Arterial inflammation is characterized by the presence of macrophages and CD4+ T lymphocytes. Activation of dendritic cells in the blood vessel adventitia-media border results in recruitment of T cells and monocytes into the vessel wall. Macrophages fuse to form giant cells, which secrete metalloproteinases and reactive oxygen species, which damage the vessel's structural integrity. In addition, intimal proliferation causes reduced blood flow and partial or complete ischaemia. Pro-inflammatory cytokine release may lead to systemic symptoms [Hoffman, 2016; Lazarewicz, 2019; Simon, 2021].
• Expert opinion in a review article notes that a 'genetic component to the development of GCA is supported by evidence of differential prevalence depending on the ethnicity, familial aggregation and multiple genetic associations' [Lyons, 2020].

How common is it?

Giant cell arteritis (GCA) is the most common form of vasculitis in people over the age of 50 years, and its incidence increases with age [Mackie, 2020a].

• A UK primary care study using data from the General Practice Research Database from 1990–2001 found [Smeeth, 2006]:
  • 3928 people had a first diagnosis of GCA during 17,830,028 person-years of observation.
  • The age-adjusted incidence rate of GCA was 2.2 per 10,000 person‐years, which remained stable during the observation period.
• A subsequent UK primary care study using data from the Clinical Practice Research Datalink from 2000–2011 (n = 4671 patients with GCA) found [Petri, 2015]:
  • The overall incidence of GCA was 1 per 10,000 person-years.
  • The highest incidence of 7.4 per 10,000 person-years was in women aged 70–79 years.
• Expert opinion in a review article states that a full-time GP is likely to see a new case of GCA every 1–2 years [Barraclough, 2012].
• Expert opinion in a review article notes that GCA typically develops after the age of 50 years, and is 2–3 times more common in women than men [Hoffman, 2016]. Another review article cites evidence from epidemiological studies in the literature that cranial GCA is more common than large vessel GCA [van der Geest, 2024]. Expert opinion in another review article notes that GCA rarely presents in people under 50 years of age, and cites evidence in the literature that the mean age of disease onset is 70 years [Lazarewicz, 2019]. 
• A meta-analysis of 107 epidemiological studies of GCA found [Li, 2021]:
  • The global pooled incidence in 61 studies was 10 cases per 100,000 people over 50 years of age.
  • The pooled prevalence in 9 studies was 51.74 cases per 100,000 people over 50 years of age.
  • The annual pooled mortality rate was 20.44 deaths per 1000 people, and mortality rates generally decreased over time.
  • The incidence varied with geographical location, with the highest incidence rates seen in people from Scandinavia, North and South America, and northern Europe.
• Expert opinion in another review article notes that people with large vessel GCA typically have disease onset at a younger age compared with people with isolated cranial involvement [Bosch, 2024]. 

What are the complications?

Inflammation in the walls of medium and large arteries in giant cell arteritis (GCA) can lead to various complications, such as:

• Loss of vision
  • Anterior ischaemic optic neuropathy is the most common mechanism for vision loss in GCA, caused by occlusion of the short posterior ciliary arteries supplying the optic nerve [Bosch, 2024].
  • Expert opinion in a review article notes that total or partial loss of vision may occur in up to 30% of people with GCA [Kermani, 2018].
  • One UK observational study (n = 271) of rheumatologist/ophthalmologist-diagnosed GCA in 8 centres found that 222 study participants had ischaemic manifestations, including vision loss, blurring, and diplopia (as well as other symptoms including jaw/tongue/limb claudication, stroke or myocardial ischaemia, or scalp necrosis). 17% of participants reported irreversible vision loss [Mackie, 2011].
  • An Italian small observational population-based cohort study (n = 136) of people with biopsy-proven GCA reported that [Salvarani, 2005]:
    • Visual symptoms (including amaurosis fugax [temporary monocular vision loss] and diplopia) developed in 41 people (30.1%).
    • Partial or total vision loss occurred in 26 people (19.1%).
    • Vision loss developed before glucocorticoid treatment in 25 of the 26 people who developed vision loss.
• Large artery complications
  • The most commonly affected large vessels are the thoracic aorta, subclavian arteries, brachiocephalic trunk, and axillary arteries [van der Geest, 2024]. Subsequent large artery complications include aortic aneurysm, aortic dissection or rupture, large artery stenosis, and aortic regurgitation [Riambau, 2017]  [Mackie, 2020a]. Large vessel involvement may present with symptoms of a systemic inflammatory syndrome, which can have features of polymyalgia rheumatica (PMR) without the typical cranial clinical features of GCA [Mackie, 2020a; van der Geest, 2024].
    • Expert opinion in a review article states that studies have found that 39% of people with large vessel GCA developed signs of aortic or other large vessel aneurysm or stenosis during a mean follow-up period of 4.4 years [van der Geest, 2024].
    • Aortic aneurysms associated with GCA often have a higher rate of growth and a higher propensity to dissect at a smaller diameter than those seen in the general population related to non-inflammatory atherosclerotic disease [Kermani, 2018].
    • Expert opinion in a review article notes that the risk of ischaemic limb claudication due to large vessel stenosis is low due to the development of a substantial collateral circulation in most affected people [Koster, 2018].
• Cardiovascular disease
  • Cardiovascular disease, including myocardial infarction, heart failure, stroke, and peripheral arterial disease, is more common in people with GCA than in the general population [Hellmich, 2020; Mackie, 2020a].
    • Vertebral artery involvement is the main cause of ischaemic stroke in people with large vessel GCA [van der Geest, 2024].
    • The European Headache Federation (EHF) consensus article cites evidence that stroke may complicate GCA in 3–10% of people [Mollan, 2020].
    • Expert opinion in a review article notes that complications such as myocardial infarction, stroke, and peripheral arterial disease more commonly present within the first month after a diagnosis of GCA [Hoffman, 2016].
• Other
  • Scalp necrosis, peripheral neuropathy, cranial nerve palsy [Bosch, 2024].
  • Adverse effects from longterm glucocorticoid treatment. See the CKS topic on Corticosteroids - oral for more information.

What is the prognosis?

The prognosis of giant cell arteritis (GCA) varies with the person's age, comorbidities, presenting symptoms, and the site of arterial involvement [Mackie, 2020a].

• Expert opinion in a review article cites evidence that incident vision loss once glucocorticoid treatment is started is rare, with rates of 1% at 5 years reported in some studies [Kermani, 2018]. Expert opinion in another review article notes that if left untreated, up to 50% of people with GCA may develop unilateral vision loss within days to weeks of symptoms starting [Lazarewicz, 2019].
  • Immediate treatment with high-dose glucocorticoids reduces the risk of permanent vision loss [Hellmich, 2020; Mackie, 2020a].
  • Expert opinion in an additional review article states that risk factors for vision loss include older age, male sex, hypertension, a positive temporal artery biopsy result, and delayed initiation of glucocorticoid treatment [Lyons, 2020].
• Most people with GCA respond rapidly to glucocorticoid treatment. However, relapses of GCA are common, and expert opinion in a review article cites evidence from retrospective studies reporting at least one relapse in 28–62% of patients, and prospective studies estimate relapses occur in 34–68% of patients [Kermani, 2018].
• The EULAR publication on large vessel GCA states that relapses are common once glucocorticoid doses are tapered, and cites evidence from several large observational cohort studies which have shown relapse rates of 34–75% in people with GCA treated with glucocorticoid therapy [Hellmich, 2020].
• The British Society for Rheumatology (BSR) guideline notes that in general, the glucocorticoid dose is usually tapered slowly over 12–18 months in most people with uncomplicated disease. Clinical features such as fever, weight loss, an erythrocyte sedimentation rate (ESR) level of more than 85 mm/h, and a haemoglobin level less than 11 g/dL may be associated with a higher relapse rate and the need for a prolonged treatment course [Mackie, 2020a].
• Expert opinion in a review article notes that men may have a lower relapse rate than women [Kermani, 2018].
• Overall, survival for people with GCA is similar to that of the general population, but the risk of developing large vessel complications such as aortic aneurysm is increased. In addition, the presence of aortic complications is associated with increased mortality rates, even in the absence of aortic dissection [Kermani, 2018].

When should I suspect a diagnosis of giant cell arteritis?

Be aware that early clinical features of giant cell arteritis (GCA) are often non-specific, and alternative causes for symptoms should be considered, depending on clinical judgement.

• Suspect a diagnosis of GCA if a person is aged 50 years or older and presents with at least one of the following:
  • New-onset localized headache.
    • Headache is the most common symptom occurring in about two-thirds of people, but it is not always present. It is usually temporal, but the location may vary, and it may be generalized, occipital, or parietal.
  • Temporal artery abnormalities, such as:
    • Tenderness, thickening, or nodularity of the superficial temporal artery; skin erythema overlying the temporal artery; reduced or absent pulsation.
  • Acute visual disturbance such as loss of vision, visual field defects, diplopia, or changes to colour vision.
    • Up to 30% of people develop vision loss that may be transient or permanent — in people with unilateral vision loss, there is a 20–50% chance of the contralateral eye also being affected.
  • Scalp tenderness or hyperaesthesia.
    • This occurs in about 50% of people, particularly over the temporal and occipital arteries, for example, when brushing hair.
    • Scalp necrosis may occur, but is less common.
  • Intermittent jaw and/or tongue claudication.
    • This occurs in nearly 50% of people, causing pain typically over the masseter muscles after minutes of chewing. Occasionally, intermittent claudication affects the tongue or the muscles involved in swallowing.
  • Systemic features.
    • Up to 50% of people with cranial GCA may present with features such as fever, sweats, fatigue, anorexia, weight loss, and depression.
  • Clinical features of polymyalgia rheumatica (PMR).
    • GCA and PMR commonly overlap. Clinical features of PMR include proximal muscle pain, stiffness, and tenderness of the shoulder and hip girdles.
    • PMR may be seen in 40–60% of people with GCA at diagnosis, and 16–21% of people with PMR may develop GCA, particularly if they are untreated. See the CKS topic on Polymyalgia rheumatica for more detailed information.
    • Imaging studies suggest that up to one-third of people with PMR have evidence of subclinical large vessel involvement at disease outset.
  • Neurological features.
    • These occur in about 30% of people and include mononeuropathy or polyneuropathy of the arms or legs; transient ischaemic attack or stroke in the distribution of the carotid or vertebrobasilar arteries; or upper cranial nerve palsies. See the CKS topic on Stroke and TIA for more information.
  • Audiovestibular or respiratory symptoms.
    • GCA may occasionally present with auditory, vestibular, or respiratory symptoms such as dry cough, sore throat, and/or hoarseness.
  • Clinical features associated with extra-cranial large vessel involvement, such as:
    • Carotid artery or other bruits.
    • Decreased arterial pulses/blood pressure difference between the arms.
    • Intermittent limb claudication (due to large vessel stenosis). See the CKS topic on Peripheral arterial disease for more information.
    • Back or chest pain due to aortitis or aortic dissection.

How should I assess a person with suspected giant cell arteritis?

If a diagnosis of giant cell arteritis (GCA) is suspected:

• Ask about:
  • Any headache, including onset, location, aggravating factors such as brushing the hair, relieving factors, and associated features.
  • Any pain when chewing or talking (jaw or tongue claudication).
  • Any visual disturbance such as loss of vision, visual field defects, diplopia, or changes to colour vision.
  • Any clinical features or known diagnosis of polymyalgia rheumatica (PMR). See the CKS topic on Polymyalgia rheumatica for more information.
  • Any symptoms of weight loss, fever, night sweats, anorexia, fatigue, limb claudication, chest, abdominal, or back pain, which may suggest extra-cranial large vessel involvement.
  • Any comorbidities which may affect the risk of glucocorticoid adverse effects, such as diabetes mellitus, hypertension, conditions which predispose to infection, glaucoma, peptic ulcer, osteoporosis, and bone fracture risk. See the CKS topics on Corticosteroids – oral and Osteoporosis - prevention of fragility fractures for more information.
  • The person's risk of cardiovascular disease. See the CKS topic on CVD risk assessment and management for more information.
  • Any clinical features suggesting an alternative diagnosis, such as focal neurological deficits, severe systemic symptoms, and/or localized ear, nose, and throat (ENT) signs.
• Examine the person.
  • Measure height, weight, body mass index (BMI), and baseline blood pressure in both arms.
  • Check the temporal artery for skin erythema, tenderness, thickening, nodularity, and/or reduced pulsation compared with the contralateral side.
  • Check for scalp tenderness or hyperaesthesia.
  • Perform an eye examination including visual acuity, visual fields, and fundoscopy to assess for pallor and oedema of the optic disc and/or a large cotton wool spot.
  • Assess for carotid, subclavian, and/or axillary artery bruits, and decreased arterial pulses/blood pressure difference between the arms suggesting extra-cranial large vessel involvement.
  • Examine for signs of limb claudication and peripheral arterial disease. See the CKS topic on Peripheral arterial disease for more information.
• Consider arranging initial investigations in primary care, unless there are clinical features of critical ischaemia (such as vision loss or diplopia) or there is no immediate access to phlebotomy.
• Do not delay initiating glucocorticoid treatment or arranging specialist referral while waiting for blood test results. The following tests may help to establish a diagnosis of GCA, but a definitive diagnosis requires specialist assessment and investigation. See the section on Initial management in Scenario: Management for more information.
  • Full blood count — normochromic normocytic anaemia and thrombocytopenia may result from inflammation.
  • C-reactive protein (CRP) — typically elevated.
  • Erythrocyte sedimentation rate (ESR) — typically elevated and often greater than 50 mm/hour, but it may be normal at presentation and even during a relapse of disease activity.
• Consider arranging additional investigations to help exclude an alternative diagnosis or to identify people at increased risk for glucocorticoid adverse effects, depending on clinical judgement, such as:
  • Serum urea and electrolytes and liver function tests.
  • Serum HbA1c to assess for diabetes mellitus. See the CKS topic on Diabetes - type 2 for more information.
  • Urine dipstick testing to check for proteinuria or haematuria, which may indicate a small vessel vasculitis.
  • Serum protein electrophoresis and urine Bence-Jones protein/serum-free light chains if the ESR is elevated out of proportion to the CRP. See the CKS topic on Multiple myeloma for more information.
  • Tests to assess risk for osteoporosis or secondary causes of osteoporosis, such as thyroid function tests, serum vitamin D and calcium level, and/or dual-energy X-ray absorptiometry (DXA) scan. See the CKS topic on Osteoporosis - prevention of fragility fractures for more information.

What else might it be?

The clinical features of giant cell arteritis (GCA) are often non-specific. Other conditions which may present similarly include:

• Other causes of headache, such as cluster headache, tension headache, or migraine. See the CKS topics on Headache – assessment, Headache – cluster, Headache - tension type, and Migraine for more information.
• Acute angle closure glaucoma. See the CKS topic on Glaucoma for more information.
• Retinal transient ischaemic attack (TIA) and embolic visual deficits. See the CKS topic on Stroke and TIA for more information.
• Temporomandibular joint pain, sinus disease, dental disease, and ear conditions such as relapsing polychondritis. See the CKS topics on TMJ disorders and Sinusitis for more information.
• Trigeminal neuralgia. See the CKS topic on Trigeminal neuralgia for more information.
• Cervical spondylosis or other upper cervical spine disease. See the CKS topics on Neck pain - cervical radiculopathy and Neck pain - non-specific for more information.
• Malignancy such as multiple myeloma, intracranial malignancy, or skull metastases. See the CKS topics on Brain and central nervous system cancers and Multiple myeloma for more information.
• Peripheral arterial disease as an atherosclerotic cause of lower limb claudication. See the CKS topic on Peripheral arterial disease for more information.
• Raynaud's phenomenon can mimic symptoms affecting the digits. See the CKS topic on Raynaud's phenomenon for more information.
• Primary vasculitides such as Takayasu arteritis, Behçet's disease, or other causes of large vessel vasculitis, such as anti-neutrophil-cytoplasm (ANCA)-associated vasculitis, granulomatosis with polyangiitis (previously known as Wegener's granulomatosis), or polyarteritis nodosa.
• Vasculitis associated with autoimmune disease such as rheumatoid arthritis, systemic lupus erythematosus, or spondyloarthritis. See the CKS topics on Axial spondyloarthritis (including ankylosing spondylitis) and Rheumatoid arthritis for more information.
• Idiopathic aortitis or aortitis related to IgG4-related disease.
• Infections, such as ophthalmic herpes zoster, syphilis, Q fever, or Mycobacterium. See the CKS topics on Shingles, Syphilis, and Tuberculosis for more information.

Scenario: Management of giant cell arteritis

From age 40 years onwards.

Search strategy

Scope of search

A literature search was conducted for guidelines and systematic reviews on primary care management of giant cell arteritis.

Search dates

August 2020 - November 2025

Key search terms

The terms listed below are the core search terms that were used for EBSCOhost MEDLINE (searched 12th August 2020). These were combined with filters to identify guidelines, systematic reviews and primary care relevant literature in EBSCOhost MEDLINE. The strategy was adapted for The Cochrane Library databases.  

S6 S1 OR S2 OR S3 OR S4 OR S5
S5 AB large vessel vasculitis OR TI large vessel vasculitis
S4 AB cranial arteritis OR TI cranial arteritis 
S3 AB temporal arteritis OR TI temporal arteritis 
S2 AB giant cell arteritis OR TI giant cell arteritis 
S1 (MH "Giant Cell Arteritis") 

Sources of guidelines

• National Institute for Health and Care Excellence (NICE)
• Scottish Intercollegiate Guidelines Network (SIGN)
• Royal College of Physicians
• Royal College of General Practitioners
• Royal College of Nursing
• NICE Evidence
• World Health Organization
• Guidelines International Network
• TRIP database
• Agency for Healthcare Research and Quality
• National Health and Medical Research Council (Australia)
• Royal Australian College of General Practitioners
• British Columbia Medical Association
• Canadian Medical Association
• Alberta Medical Association
• Michigan Quality Improvement Consortium
• Singapore Ministry of Health
• National Resource for Infection Control
• RefHELP NHS Lothian Referral Guidelines
• Medline (with guideline filter)
• Driver and Vehicle Licensing Agency
• NHS Health at Work (occupational health practice)

Sources of systematic reviews and meta-analyses

• The Cochrane Library:
  • Systematic reviews
  • Protocols
  • Database of Abstracts of Reviews of Effects
• Medline (with systematic review filter)
• EMBASE (with systematic review filter)

Sources of health technology assessments and economic appraisals

• NIHR Health Technology Assessment programme
• The Cochrane Library:
  • NHS Economic Evaluations
  • Health Technology Assessments
• Canadian Agency for Drugs and Technologies in Health
• International Network of Agencies for Health Technology Assessment

Sources of randomized controlled trials

• The Cochrane Library:
  • Central Register of Controlled Trials
• Medline (with randomized controlled trial filter)
• EMBASE (with randomized controlled trial filter)

Sources of evidence based reviews and evidence summaries

• Drug and Therapeutics Bulletin
• TRIP database
• Central Services Agency COMPASS Therapeutic Notes

Sources of national policy

• Department of Health
• Health Management Information Consortium (HMIC)

Patient experiences

• Healthtalk
• BMJ - Patient Journeys

Sources of medicines information

The following sources are used by CKS pharmacists and are not necessarily searched by CKS information specialists for all topics. Some of these resources are not freely available and require subscriptions to access content.

• British National Formulary (BNF)
• electronic Medicines Compendium (eMC)
• European Medicines Agency (EMEA)
• Medicines and Healthcare products Regulatory Agency (MHRA)
• REPROTOX
• Scottish Medicines Consortium
• Stockley's Drug Interactions
• TERIS
• TOXBASE
• Micromedex
• UK Medicines Information

Stakeholder engagement

Our policy

The external review process is an essential part of CKS topic development. Consultation with a wide range of stakeholders provides quality assurance of the topic in terms of:

• Clinical accuracy.
• Consistency with other providers of clinical knowledge for primary care.
• Accuracy of implementation of national guidance (in particular NICE guidelines).
• Usability.

Principles of the consultation process

• The process is inclusive and any individual may participate.
• To participate, an individual must declare whether they have any competing interests or not. If they do not declare whether or not they have competing interests, their comments will not be considered.
• Comments received after the deadline will be considered, but they may not be acted upon before the clinical topic is issued onto the website.
• Comments are accepted in any format that is convenient to the reviewer, although an electronic format is encouraged.
• External reviewers are not paid for commenting on the draft topics.
• Discussion with an individual or an organization about the CKS response to their comments is only undertaken in exceptional circumstances (at the discretion of the Clinical Editor or Editorial Steering Group).
• All reviewers are thanked and offered a letter acknowledging their contribution for the purposes of appraisal/revalidation.
• All reviewers are invited to be acknowledged on the website. All reviewers are given the opportunity to feedback about the external review process, enabling improvements to be made where appropriate.

Stakeholders

• Key stakeholders identified by the CKS team are invited to comment on draft CKS topics. Individuals and organizations can also register an interest to feedback on a specific topic, or topics in a particular clinical area, through the Getting involved section of the Clarity Informatics website.
• Stakeholders identified from the following groups are invited to review draft topics:
  • Experts in the topic area.
  • Professional organizations and societies (for example, Royal Colleges).
  • Patient organizations, Clarity has established close links with groups such as Age UK and the Alzheimer’s Society specifically for their input into new topic development, review of current topic content and advice on relevant areas of expert knowledge.
  • Guideline development groups where the topic is an implementation of a guideline.
  • The British National Formulary team.
  • The editorial team that develop MeReC Publications.
• Reviewers are provided with clear instructions about what to review, what comments are particularly helpful, how to submit comments, and declaring interests.

Patient engagement

Clarity Informatics has enlisted the support and involvement of patients and lay persons at all stages in the process of creating the content which include:

• Topic selection
• Scoping of topic
• Selection of clinical scenarios
• First draft internal review
• Second draft internal review
• External review
• Final draft and pre-publication

Our lay and patient involvement includes membership on the editorial steering group, contacting expert patient groups, organizations and individuals.

Evidence exclusion criteria

Our policy

Scoping a literature search, and reviewing the evidence for CKS is a methodical and systematic process that is carried out by the lead clinical author for each topic. Relevant evidence is gathered in order that the clinical author can make fully informed decisions and recommendations. It is important to note that some evidence may be excluded for a variety of reasons. These reasons may be applied across all CKS topics or may be specific to a given topic.

Studies identified during literature searches are reviewed to identify the most appropriate information to author a CKS topic, ensuring any recommendations are based on the best evidence. We use the principles of the GRADE and PICOT approaches to assess the quality of published research. We use the principles of AGREE II to assess the quality of published guidelines.

Standard exclusions for scoping literature:

• Animal studies
• Original research is not written in English

Possible exclusions for reviewed literature:

• Sample size too small or study underpowered
• Bias evident or promotional literature
• Population not relevant
• Intervention/treatment not relevant
• Outcomes not relevant
• Outcomes have no clear evidence of clinical effectiveness
• Setting not relevant
• Not relevant to UK
• Incorrect study type
• Review article
• Duplicate reference

Organizational, behavioural and financial barriers

Our policy

The CKS literature searches take into consideration the following concepts, which are discussed at the initial scoping of the topic.

• Feasibility
  • Studies are selected depending on whether the intervention under investigation is available in the NHS and can be practically and safely undertaken in primary care.
• Organizational and Financial Impact Analysis
• Studies are selected and evaluated on whether the intervention under investigations may have an impact on local clinical service provision or national impact on cost for the NHS. The principles of clinical budget impact analysis are adhered to, evaluated and recorded by the author. The following factors are considered when making this assessment and analysis.
  • Eligible population
  • Current interventions
  • Likely uptake of new intervention or recommendation
  • Cost of the current or new intervention mix
  • Impact on other costs
  • Condition-related costs
  • In-direct costs and service impacts
  • Time dependencies
• Cost-effectiveness or cost-benefit analysis studies are identified where available. 

We also evaluate and include evidence from NICE accredited sources which provide economic evaluations of recommendations, such as NICE guidelines. When a recommended action may not be possible because of resource constraints, this is explicitly indicated to healthcare professionals by the wording of the CKS recommendation.

Declarations of interest

Our policy

Clarity Informatics requests that all those involved in the writing and reviewing of topics, and those involved in the external review process to declare any competing interests. Signed copies are securely held by Clarity Informatics and are available on request with the permission of the individual. A copy of the declaration of interest form which participants are asked to complete annually is also available on request. A brief outline of the declarations of interest policy is described here and full details of the policy is available on the Clarity Informatics website. Declarations of interests of the authors are not routinely published, however competing interests of all those involved in the topic update or development are listed below. Competing interests include:

• Personal financial interests
• Personal family interest
• Personal non-financial interest
• Non-personal financial gain or benefit

Although particular attention is given to interests that could result in financial gains or losses for the individual, competing interests may also arise from academic competition or for political, personal, religious, and reputational reasons. An individual is not obliged to seek out knowledge of work done for, or on behalf of, the healthcare industry within the departments for which they are responsible if they would not normally expect to be informed.

Who should declare competing interests?

Any individual (or organization) involved in developing, reviewing, or commenting on clinical content, particularly the recommendations should declare competing interests. This includes the authoring team members, expert advisers, external reviewers of draft topics, individuals providing feedback on published topics, and Editorial Steering Group members. Declarations of interest are completed annually for authoring team and editorial steering group members, and are completed at the start of the topic update and development process for external stakeholders.

Competing interests declared for this topic:

None.