Changes

October 2025 — reviewed. A literature search was conducted in September 2025 to identify evidence-based guidelines, UK policy, systematic reviews and key randomized controlled trials published since the last version of this topic. No major changes to clinical recommendations have been made.

Update

Goals

To support primary healthcare professionals to:

• Detect and diagnose hyponatraemia.
• Arrrange emergency hospital admission or specialist referral if clinically appropriate depending on duration and severity.
• Determine the likely underlying cause, if possible and clinically appropriate.
• Offer management in primary care for mild asymptomatic hyponatraemia, depending on clinical judgement.

Outcome measures

Audit criteria

QOF indicators

QIPP - Options for local implementation

NICE quality standards

What is it?

• Hyponatraemia is defined as a water balance disorder, when the serum sodium concentration is less than 135 mmol/L [Spasovski, 2014] [Tinawi, 2020] [Ball, 2022].
  • Normal serum sodium concentration is in the range of 135–145 mmol/L.
• The severity of hyponatraemia can be classified as [Spasovski, 2014] [Tinawi, 2020] [Ball, 2022]:
  • Mild — serum sodium concentration 130–135 mmol/L.
  • Moderate — serum sodium concentration 125–129 mmol/L.
  • Severe — serum sodium concentration less than 125 mmol/L.
• The rate of onset of hyponatraemia can be classified as [Spasovski, 2014] [Jacob, 2019] [Tinawi, 2020]: 
  • Acute — duration of less than 48 hours.
  • Chronic — duration of 48 hours or more.
  • Unknown — in practice, most cases of hyponatraemia are of undetermined duration and should be considered chronic, unless there is clinical evidence suggesting otherwise [Jacob, 2019; Seay, 2020].
• Hyponatraemia can also be classified according to serum osmolality as [Sahay, 2014] [Spasovski, 2014] [Seay, 2020]:
  • Hypertonic or hyperosmolar hyponatraemia (high serum osmolality).
  • Pseudo-hyponatraemia or isotonic hyponatraemia (normal serum osmolality).
  • Hypotonic or true hyponatraemia (low serum osmolality). This is more common than hypertonic or pseudo-hyponatraemia, and can be further classified by volume status as:
    • Hypovolaemic hyponatraemia (volume depletion).
    • Hypervolaemic hyponatraemia (volume overload).
    • Euvolaemic hyponatraemia (normal volume status).

What is the pathophysiology?

Overall body fluid concentration is regulated within a narrow range, and abnormalities in overall effective body fluid concentration, or tonicity, present as disturbances in serum sodium concentration [Seay, 2020]. The underlying mechanism leading to hyponatraemia depends on the underlying cause(s).

• Hyponatraemia results from a relative excess of body water compared with total body sodium [Spasovski, 2014].
  • Serum sodium concentration is determined by serum water content. Serum water increases with water intake (driven by thirst or habit) and decreases through insensible losses (for example, sweating) and urinary dilution [Seay, 2020].
  • Urinary dilution is regulated mainly by the antidiuretic hormone (ADH) also known as vasopressin [Spasovski, 2014]. ADH is produced by the hypothalamus and then stored in and released from the posterior pituitary gland. It increases the reabsorption of water by the collecting duct of the kidney, concentrates the urine, and prevents excessive loss of water from the body [Spasovski, 2014; Seay, 2020].
  • Usually, osmotic regulation of the release of ADH from the posterior pituitary gland primarily depends on the effective osmolality of the serum [Spasovski, 2014]. ADH is also secreted in response to decreased effective arterial blood volume [Adrogue, 2022].
• Hyponatraemia is usually associated with a disturbance in ADH secretion [Spasovski, 2014]. This can be:
  • Physiological (for example, due to hypovolaemia).
  • Pathological (for example, due to heart failure).
  • Iatrogenic (for example, due to the use of medication such as thiazide diuretics).
• In most cases of hyponatraemia, there is an inability to suppress ADH. In rare cases, ADH is suppressed for other reasons. See the section on Causes for more information.

What causes it?

Hyponatraemia is primarily a disorder of water balance, and may be caused by a wide variety of underlying conditions, based on different pathophysiological mechanisms, which may co-exist [Spasovski, 2014] [Woodward, 2018] [Adrogue, 2022] [Sumi, 2025].

• Hypotonic (or true) hyponatraemia can result from a range of clinical conditions that can be categorized by their effect on extracellular fluid volume [Saeed, 2014; Spasovski, 2014; Dineen, 2017; Woodward, 2018; Seay, 2020; Tinawi, 2020].
  • Hypovolaemic (volume depletion) hyponatraemia occurs when the total body water and sodium content are both decreased, but the relative decrease in total body sodium is greater than the decrease in total body water. Possible causes include [Spasovski, 2014; Woodward, 2018; Adrogue, 2022]:
    • Medications, especially thiazide and thiazide-like diuretics — these may induce the release of antidiuretic hormone (ADH) or increase the response to circulating ADH.
    • Endocrine disorders, such primary adrenal insufficiency (Addison's disease), where hypoaldosteronism results in increased excretion of sodium in the urine.
    • Cerebral salt-wasting (rare) resulting from intracranial pathology such as subarachnoid haemorrhage, traumatic brain injury, or intracranial surgery. Elevated levels of atrial and/or brain natriuretic peptide cause an increase in renal sodium loss.
    • Severe diarrhoea and/or vomiting (gastrointestinal sodium loss).
    • Sweating (may be impaired reabsorption of sodium in the sweat duct) or extensive skin burns (impaired natural barrier function causing sodium and volume depletion).
    • Sodium-losing nephropathy, for example, polycystic kidney disease, chronic pyelonephritis, or tubulopathy after chemotherapy, can inhibit the kidney's ability to reabsorb appropriate amounts of sodium.
    • 'Third space' losses where excess fluid leaks from blood vessels into the interstitial space (for example, due to bowel obstruction, pancreatitis, severe hypoalbuminaemia, sepsis, or muscle trauma). The reduced effective blood volume can activate baroreceptor-mediated ADH release, leading to water retention.
  • Hypervolaemic (volume overload) hyponatraemia occurs when the total body water and sodium content both increase, but the relative increase in total body water is greater than the increase in total body sodium, resulting in oedema. Possible causes include [Spasovski, 2014; Adrogue, 2022]:
    • Heart failure — low cardiac output stimulates sodium and water retention by the increased secretion of ADH by the pituitary.
    • Liver disease (such as cirrhosis with ascites) — reduced effective arterial blood volume from decreased vascular resistance can activate baroreceptor-mediated ADH release, leading to water retention.
    • Kidney disease — if glomerular filtration rate reduces or there is tubular injury or scarring, there is a reduced ability to dilute urine and excrete free water. In nephrotic syndrome, blood volume may be reduced due to lower serum oncotic pressure, resulting in stimulation of ADH secretion.
  • Euvolaemic (normal volume status) hyponatraemia occurs when the total body water increases but the total body sodium remains unchanged. This results from an excessive fluid intake in the presence of impaired free water excretion, either due to inappropriate release of ADH or a low intake of solutes. Possible causes include [Spasovski, 2014; Jacob, 2019; Seay, 2020; Adrogue, 2022; Ball, 2022]:
    • Syndrome of inappropriate antidiuresis (SIAD) — characterized by excessive unsuppressible release of ADH either from the posterior pituitary or ectopic production from an abnormal non-pituitary source, independent of serum osmolality or circulating volume. This is a diagnosis of exclusion. SIAD may be caused by drugs that increase the production, or potentiate the action of ADH, such as selective serotonin reuptake inhibitors, tricyclic antidepressants, opioids, thiazide diuretics, angiotensin-converting enzyme (ACE) inhibitors and angiotensin-II receptor antagonists, proton pump inhibitors, antiseizure medication, antipsychotics, theophylline, amiodarone, methotrexate, nonsteroidal anti-inflammatory drugs, dopamine agonists, and 3,4-methylenedioxymethamphetamine (MDMA), commonly known as ecstasy. It can also result from malignancy (such as small cell lung cancer, gastrointestinal tract cancers), central nervous system disorders (such as subarachnoid haemorrhage, meningitis, encephalitis), pneumonia, or other non-specific causes, including pain, nausea, acute stress, including exercise, post-operatively, or can be idiopathic.
    • Endocrine disorders — secondary adrenal insufficiency is caused by reduced or absent secretion of adrenocorticotropic hormone. This results in persistently low concentrations of cortisol, which fail to suppress ADH, causing impaired free water excretion. In addition, very rarely, severe hypothyroidism may cause hyponatraemia, possibly due to reduced cardiac output and glomerular filtration rate.
    • High water, low solute intake — in primary polydipsia, the osmotic threshold for thirst is reduced below the threshold for the release of ADH, resulting in excess water intake despite a low plasma osmolality (seen in some psychiatric conditions such as psychosis). Hyponatraemia may also result if solute intake is low relative to water intake, such as in anorexia nervosa, 'tea and toast' diet, and beer potomania (excess beer consumption with a low solute diet).
    • Reset osmostat syndrome — there may be a reduced threshold for the release of ADH when it is secreted at a lower plasma osmolality, which impairs renal excretion of excess water. The corrective mechanism to re-establish normal serum sodium concentration occurs at a lower threshold, resulting in chronic stable hyponatraemia, for example, due to pregnancy or tuberculosis.
• Pseudo-hyponatraemia describes a laboratory artefact low serum sodium concentration due to hyperproteinaemia (for example, due to multiple myeloma) or hypertriglyceridaemia (for example, due to pancreatitis or diabetic ketoacidosis). The abnormally high concentrations of proteins or lipids in the blood interfere with the accurate measurement of sodium [Spasovski, 2014; Spasovski, 2024].
• Hypertonic (or hyperosmolar) hyponatraemia can be caused by severe hyperglycaemia (hyperosmolality causes dilution due to movement of intracellular water into the extracellular space) [Spasovski, 2014; Adrogue, 2022].

What are the risk factors?

• Thiazide diuretics induce hyponatraemia in up to 30% of affected people. Additional risk factors for people taking diuretics include [Spasovski, 2014] [Woodward, 2018] [Adrogue, 2022] [Lindner, 2022]:
  • Increasing age — including polypharmacy (including concurrent use of antidepressant or antipsychotic medication), comorbidities such as heart failure, and physiological changes such as a reduced renal diluting capacity.
  • Female sex.
  • Low body mass index (BMI).
  • Low sodium intake.
  • Increased risk of hospitalization — hyponatraemia can be present on admission to hospital, or can develop (or worsen) during admission, as a result of factors such as organ failure, medications, or the post-operative state.

How common is it?

Hyponatraemia is the most common electrolyte disorder encountered in clinical practice [Spasovski, 2014].

• The joint European Society of Intensive Care Medicine (ESICM), the European Society of Endocrinology (ESE), and the European Renal Association-European Dialysis and Transplant Association (ERA-EDTA) clinical practice guideline on hyponatraemia states that it is estimated to occur in 15–20% of emergency hospital admissions [Spasovski, 2014].
• Expert opinion in a review article cites evidence that over 40% of elderly patients admitted to intensive care experience hyponatraemia at some time during their hospitalization, and chronic hyponatraemia is seen in 18% of elderly care home residents [Woodward, 2018].
• A cross-sectional French study investigated the prevalence of mild hyponatraemia and its association with falls in older adults (aged 75 years and over) admitted to an emergency elderly care medical unit. Of 696 cases, the prevalence of mild hyponatraemia was 15.9%. The prevalence rate of mild hyponatraemia was 13.2% in people without falls and 26.1% in people admitted for falls. It concluded that mild hyponatraemia was significantly associated with falls, with an adjusted odds ratio of 3.02 [Boyer, 2019].
• A Malaysian study of electronic medical records identified people aged 60 years and over with a serum sodium of less than 135 mmol/L attending an outpatient clinic. Of the 5873 people identified, 403 people (6.9%) had hyponatraemia on at least one blood test. Medical records were available for 253 people, and of these, 178 people (70.4%) had mild hyponatraemia and 75 people (29.6%) had moderate-to-severe hyponatraemia [Tay, 2019].

What are the complications?

Possible complications of hyponatraemia include:

• Brain and neurological
  • Cerebral oedema is a potentially life-threatening complication of severe and/or acute-onset hyponatraemia. It can present with symptoms of raised intracranial pressure, such as vomiting, headache, drowsiness, seizures, coma, and cardio-respiratory arrest due to cerebral herniation [Spasovski, 2014; Dineen, 2017].
  • If hyponatraemia is chronic and there is an over-rapid correction of the serum sodium concentration, 'osmotic demyelination syndrome' may develop, typically 2–6 days later, with potential irreversible brain damage [Spasovski, 2014; Sumi, 2025]. Clinical features include pseudobulbar palsy (dysarthria and dysphagia), hyper-reflexia, Parkinsonism, quadriparesis, disorientation, coma, and possible death [Seay, 2020; Tinawi, 2020; Adrogue, 2022; Sumi, 2025]. The risk relates to the speed of increase in serum sodium concentration, and also other factors including alcohol misuse, malnutrition, advanced liver disease, use of thiazide diuretics or antidepressant medication, hypokalaemia, and increased severity and duration of hyponatraemia [Spasovski, 2014; Seay, 2020; Tinawi, 2020; Adrogue, 2022].
• Bone
  • Bone complications associated with chronic hyponatraemia include gait disturbance, increased risk of falls, fragility fractures, and osteoporosis (increased risk with increased severity of hyponatraemia) [Spasovski, 2014; Jacob, 2019; Kheetan, 2021; Adrogue, 2022].
• Lung
  • Non-cardiogenic pulmonary oedema can complicate hyponatraemia due to acute water intoxication during endurance sports, for example, or drug intoxication with ecstasy. Subsequent hypoxaemia can increase the risk of cerebral oedema [Adrogue, 2022].
• Hospitalization and mortality
  • In hospitalized people, hyponatraemia is associated with an increased risk of morbidity, mortality, increased length of hospital admission, and higher risk of re-admission compared with people with normal serum sodium concentrations. It is uncertain whether this relates to the hyponatraemia itself, or the underlying comorbidities, and/or medications [Corona, 2013; Spasovski, 2014; Corona, 2016].
  • The prognosis of hyponatraemia depends on its severity and underlying cause(s), and is often poor in acute, severe hyponatraemia, particularly in older people [Spasovski, 2014].

When should I suspect hyponatraemia?

Hyponatraemia is usually an incidental finding on routine blood tests. Most people are asymptomatic, particularly if hyponatraemia is mild and of gradual onset.

• Symptoms (if present) are often non-specific, and are related to the severity of hyponatraemia, its rate of onset, duration, the intrinsic ability of the brain and central nervous system to adapt to changing osmolar stress, and the range and degree of any comorbidities.
• Symptoms are more common in people with acute hyponatraemia than chronic hyponatraemia.
  
  • Rapid changes in serum sodium concentrations or severe hyponatraemia can cause symptoms such as vomiting, drowsiness, headache, seizures, coma, and cardio-respiratory arrest due to cerebral oedema and raised intracranial pressure.
  • Moderately severe hyponatraemia may cause nausea without vomiting, lethargy, fatigue, disorientation, confusion, and headache.
  • Mild chronic hyponatraemia can lead to gait disturbance, risk of falls, reduced concentration, irritability, altered mood, and other cognitive deficits.
• The severity of clinical symptoms may not correlate with the degree of hyponatraemia.
  • People with severe hyponatraemia may be asymptomatic, while some people with moderate hyponatraemia may have significant neurological symptoms and signs.
  • Be aware that severe symptoms are unlikely with serum sodium concentrations greater than 130 mmol/L, and if there are signs of neurological deficit, consider alternative causes for symptoms.

How should I assess a person with hyponatraemia?

If a person has moderate or severe hyponatraemia and/or any symptoms, see the section on Admission or referral for more information on management. If a person has asymptomatic, mild hyponatraemia, assess to identify any underlying cause(s) and the person's volume status to guide management.

• Ask about:
  
  • Any acute intercurrent illness (such as gastroenteritis) and duration of illness, or recent surgery.
  • Fluid intake, thirst levels, urine output, and changes in body weight.
  • Any medication, such as diuretics. Be aware that the use of diuretics does not exclude other or additional causes of hyponatraemia.
  • Any contributory comorbidities or long-term conditions.
  • Lifestyle factors including exercise (including prolonged running, endurance sports), diet and nutrition, alcohol intake, and recreational drug use.
  • Any previous episodes of hyponatraemia or known chronic hyponatraemia.
• Examine the person:
  • Assess pulse rate, lying and standing blood pressure, jugular venous pressure, any oedema, and any additional signs of dehydration or fluid overload to assess volume status and help identify the underlying cause.
    
    • Hypovolaemia is characterized by tachycardia, postural hypotension, dry skin and mucous membranes, low urine output, decreased jugular venous pressure, and reduced skin turgor.
    • Hypervolaemia is characterized by peripheral, sacral, and/or pulmonary oedema and/or ascites, significant weight gain, and raised jugular venous pressure.
• Arrange investigations in primary care, depending on clinical judgement. See the section on Interpreting investigation results for more information.
  • Repeat the serum sodium concentration with potassium, urea, and creatinine levels, the timescale depending on clinical judgement, to exclude a rapidly decreasing serum sodium concentration, which will require hospital admission. See the section on Admission or referral for more information.
  • Measure serum osmolality to differentiate between hypotonic (true) hyponatraemia, hypertonic hyponatraemia, and pseudo-hyponatraemia.
  • Send a urine sample at the same time as blood samples, to measure urinary osmolality and sodium concentration.
    • Urinary osmolality provides an estimate of antidiuretic hormone (ADH) activity and can be used to evaluate the cause of hyponatraemia.
    • Urinary sodium concentration in conjunction with the person's volume status may help differentiate the underlying cause of hyponatraemia.
  • Consider arranging additional investigations to help identify an underlying cause, such as:
    
    • Urinalysis for urine protein and blood, serum estimated glomerular filtration rate (eGFR) and creatinine, and urine albumin:creatinine ratio (ACR) — if kidney disease is suspected. See the CKS topics on Acute kidney injury and Chronic kidney disease for more information.
    • Blood glucose and/or HbA1c level — to exclude hyperglycaemia as a cause of hypertonic (or hyperosmolar) hyponatraemia. See the CKS topics on Diabetes - type 1 and Diabetes - type 2 for more information on interpreting blood glucose and HbA1c results.
    • Thyroid function tests — if hypothyroidism is suspected. See the CKS topic on Hypothyroidism for more information.
    • 9am serum cortisol — if adrenal insufficiency such as Addison's disease is suspected. See the CKS topic on Addison's disease for more information.
    • B-type natriuretic peptide — if heart failure is suspected.  See the CKS topic on Heart failure - chronic for more information.
    • Liver function tests — if liver disease is suspected. See the CKS topics on Cirrhosis and Jaundice in adults for more information. Woodward 2020
    • Lipid levels and/or myeloma screen — if a diagnosis of pseudohyponatraemia is suspected. See the CKS topics on Lipid modification - CVD prevention and Multiple myeloma for more information.

Scenario: Management

From age 18 years onwards.

Search strategy

Scope of search

A literature search was conducted for guidelines, systematic reviews and randomized controlled trials on primary care management of hyponatraemia.

Search dates

October 2020 - September 2025

Key search terms

Various combinations of searches were carried out. The terms listed below are the core search terms that were used for Medline.

• Hyponatremia/

• Hyponatremia.ti,ab. or Hyponatraemia.ti,ab. or Hyponatremias.ti,ab.

• Also included :Syndrome of Inappropriate ADH/ (SIADH)
  

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.