clinical management guideline for acute hyperkalaemia...3-lead ecg monitoring should be initiated...

Clinical Management Guideline For Acute Hyperkalaemia Written by: Cross Site Lead for Critical Care Review date: March 2018 RWF-OPG-PS16 Document issue no.: 1.0 of 17

MAIDSTONE AND TUNBRIDGE WELLS NHS TRUST

Clinical Management Guideline for Acute Hyperkalaemia

Requested/ Required by: Resuscitation Committee

Main author: Dr James Wood, Cross Site Lead for Critical Care

Other contributors: Resuscitation Officer Maidstone

Document lead: Cross Site Lead for Critical Care

Directorate: Acute Services

Specialty: Critical Care

Supersedes: N/A – new document

Approved by: Resuscitation Committee, 14th December 2015

Ratified by: Clinical Guideline Ratification Group on behalf of Trust Clinical Governance Committee, 21st March 2016

Review date: March 2018

Disclaimer: Printed copies of this document may not be the most recent version. The master copy is held on Q-Pulse Document Management System

This copy – REV1.0


Document history

Requirement for document:

To ensure best practice in the management of hyperkalaemia

Cross references:

Treatment of Acute Hyperkalaemia in Adults UK Renal Association (March 2014)

Guys and St Thomas’ NHS Foundation Trust (GSTFT) Clinical Management Guideline for Patients with Hyperkalaemia. Version 1 (May 2008).

Guidelines for the treatment of hyperkalaemia in adults. (January 2006) www.crestni.org.uk

GSTFT Hypoglycaemia Treatment guideline (March 2008): http://tww-apps/cgg/CGGdetail.asp?CGG=224

Associated documents:

Version control:

Issue: Description of changes: Date:

1.0 This is first issue of this guideline March 2016

http://www.crestni.org.uk/

http://tww-apps/cgg/CGGdetail.asp?CGG=224


Clinical Management Guideline for Hyperkalaemia Contents Page

1.0 Introduction and scope 5

2.0 Definitions 5

3.0 Duties 5

4.0 Training / competency requirements 5

5.0 Signs and symptoms of hyperkalaemia 6

5.1 Causes of hyperkalaemia 6

5.2 Assessment of the patient 6

5.3 Monitoring the patient 7

5.4 Treatment of hyperkalaemia 8

5.5 Referral and transfer 12

6.0 Review potentially offending medications 12

7.0 Post incident checklist 13

8.0 Clinical pearls 13

9.0 Monitoring and audit 14

Appendix 1: Process requirements 15 1.0 Implementation and awareness 15 2.0 Review 15 3.0 Archiving 15

Appendix 2: Consultation table 16

Appendix 3: Equality impact assessment 17


1.0 Introduction and scope Hyperkalaemia occurs when the extracellular potassium ion [K+] concentration is above the normal value. It is a potentially life-threatening emergency that can be corrected with treatment. It has relevance to all clinicians and is encountered in a variety of clinical settings.

There is no universal definition of hyperkalaemia, but a serum K+ ≥ 5.5 mmol/L is widely used. Hyperkalaemia is a spectrum with the incidence of complications rising with increasing severity of hyperkalaemia and the rate of rise of serum potassium. It is potentially life threatening resulting in cardiac conduction abnormalities, arrhythmias and death.

The reported incidence of hyperkalaemia in hospitalised patients is between 1 and 10%, with the majority of cases related to prescription medication (often longstanding), in association with chronic or acute kidney injury. Most other cases are related to potassium supplementation and prescription of diuretics/drugs with potassium-sparing properties.

This guideline covers the common causes of hyperkalaemia, and its management in adult patient groups. It does NOT apply to the management of hyperkalaemia in diabetic ketoacidosis (follow DKA guideline)

2.0 Definitions

Hyperkalaemia according to UK Renal Association Clinical Practice Guidelines and the European Resuscitation Council Guideline is classified as:

Mild: (K+ 5.5 – 5.9 mmol/L)

Moderate: (K+ 6. - 6.4 mmol/L) or

Severe: (K+ ≥ 6.5 mmol/L) or if ECG changes or symptoms (muscle weakness, flaccid paralysis palpitations, or paresthesias) are present at ANY level or serum potassium ≥5.5mmol/l especially if associated with hypoxia

3.0 Duties

All patients developing hyperkalaemia in hospital should be assessed and the hyperkalaemia treated to ensure their safety. The precipitating cause for the hyperkalaemia must also be identified and managed, and the details of this process included in their discharge summary.

4.0 Training / competency requirements

All doctors, and nurses working in renal, cardiac or acute care settings are educated in the recognition, treatment, potential hazards and prevention of hyperkalaemia. Whilst there are no specific training recommendations, professionals should keep themselves updated appropriately.


5.0 Signs and symptoms of hyperkalaemia

Arrhythmias

Muscle weakness

Constipation

ECG changes (peaked T waves, loss of P waves, widening of QRS complexes, PR prolongation, asystole). However ECG changes may be modified by the presence of co-existing metabolic disorders such as metabolic acidosis, calcium concentration, sodium concentration, and the rate of rise of serum K+

5.1 Causes of hyperkalaemia

Pseudohyperkalaemia

Prolonged tourniquet time

Test tube haemolysis

Marked leucocytosis and thrombocytosis (measure plasma not serum concentration in these disease states by using a lithium heparin bottle which has a green cap and black ring)

Sample taken from a limb infused with IV fluids containing potassium

Transcellular shift (intracellular to extracellular compartment)

Acidosis (including diabetic ketoacidosis)

Drugs (digoxin toxicity, succinylcholine, arginine, β-blockade)

Renal causes

Acute or chronic renal failure

Hyperkalaemic renal tubular acidosis (type IV)

Mineralocorticoid deficiency (hypoaldosteronism states / Addisons)

Drugs that interfere with potassium excretion (amiloride, spironolactone)

Drugs that interfere with the renin-angiotensin system (ACE inhibitors, angiotensin II receptor blockade, NSAIDs, heparin)

Increase circulating potassium - exogenous or endogenous

Exogenous (potassium supplementation)

Endogenous (tumour lysis syndrome, rhabdomyolysis, trauma, burns)

Please note that this list is not comprehensive and that other causes may need to be considered.

5.2 Assessment of the patient

All patients with known or suspected hyperkalaemia should undergo urgent assessment by nursing and medical staff to assess clinical status using the ABCDE approach, an early warning scoring system used, and an appropriate escalation plan bearing in mind that the first presentation may be an arrhythmia. A comprehensive medical and drug history and clinical examination to determine the cause of hyperkalaemia should be performed.

All patients with a serum K+ value ≥ 6.0 mmol/L should have an urgent 12-lead ECG performed and assessed for changes associated with hyperkalaemia.


Is this “true” hyperkalaemia?

The lab range for a “normal” potassium is 3.5-5.0mmol/L, so a result above 5.0mmol/L is classed as hyperkalaemia. A repeat serum potassium should be ordered urgently to exclude pseudohyperkalaemia, especially if hyperkalaemia is an unexpected or isolated finding and there are no ECG signs of hyperkalaemia. A venous or arterial blood gas may provide a rapid re-assessment of the serum potassium and may help elucidate its cause.

How severe is the hyperkalaemia?

Hyperkalaemia is classified as –

Mild: (K+ 5.5 – 5.9 mmol/L)

Moderate: (K+ 6. - 6.4 mmol/L) or

Severe: (K+ ≥ 6.5 mmol/L) or if ECG changes or symptoms (muscle weakness, flaccid paralysis palpitations, or paresthesias) are present at ANY level or serum potassium ≥5.5mmol/l especially if associated with hypoxia

Is urgent treatment required?

Urgent treatment is required if:

hyperkalaemia is accompanied by ECG changes or symptoms listed above - even in the presence of mild hyperkalaemia (K+ 5.5 - 6.0) OR

the serum potassium is ≥7.0 mmol/l

Why has the patient got hyperkalaemia?

A thorough medical history focussing on a history of renal disease and determination of the medications or fluids prescribed will often reveal the cause of the hyperkalaemia. Examine for bladder distension and prostatic hypertrophy. Catheterise if appropriate. Patients receiving treatment for heart failure can develop hyperkalaemia when relative dehydration occurs.

5.3 Monitoring the patient

A 12-lead ECG should be performed in all patients suspected of having hyperkalaemia.

The ECG does not always demonstrate changes, even in the presence of severe hyperkalaemia, so a normal ECG does not obviate the need for therapy. However, the presence of ECG findings should be a strong impetus for urgent action

The most worrying findings are decreased or absent P-waves, PR prolongation, QRS widening, sine wave QRST, AV dissociation or asystole. It is often difficult to judge if T-waves are truly peaked and this finding on its own should not be an automatic indication for urgent therapy Monitor urea, electrolytes and glucose at regular intervals. Additional blood work including creatinine kinase and blood gas analysis should be performed if appropriate.

Situations associated with a rapid rise in potassium (acute renal failure, rhabdomyolysis) and hypoxia of any cause are more strongly associated with the development of cardiac conduction disturbances. Mild hyperkalaemia is common and often well tolerated in patients with chronic renal failure


3-lead ECG monitoring should be initiated for all patients with a serum K+ value ≥ 6.5 mmol/L, patients with features of hyperkalaemia on 12-lead ECG, and in patients with a serum K+ value between 6.0-6.4 mmol/L who are clinically unwell or in whom a rapid rise in serum K+ is anticipated, ideally in a high-dependency setting.

Figure 1: ECG in a patient with severe hyperkalaemia (serum K+ 9.1 mmol/L) illustrating peaked T waves (a), diminished P waves (b) and wide QRS complexes (c).

5.4 Treatment of hyperkalaemia

5.4.1 Initial treatment of hyperkalaemia should follow a logical 5-step approach (based upon the recommendations of the Renal Association):

1. Protect the heart; by intravenous administration of calcium salts 10ml 10% calcium chloride or 10 mls of 10% calcium gluconate should be given over 3 minutes to patients with hyperkalaemia. This may be repeated as required in the presence of ECG evidence of hyperkalaemia. (see 5.4.2)


2. Shift K+ into cells; using insulin-glucose infusion (10 units soluble insulin in 50ml of 50% dextrose 25g glucose) by intravenous infusion over 15-30 minutes into a large vein to treat moderate or severe hyperkalaemia (K+ ≥ 6.0 mmol/L). Nebulised Salbutamol should be used as an adjunctive treatment for moderate or severe hyperkalaemia but must not be used as a monotherapy.

3. Remove K+ from the body; cation-exchange resins these should not be used in the emergency treatment of severe hyperkalaemia, but may be considered in patients with mild to moderate hyperkalaemia. The patients renal function should be optimised by rehydration if they are dehydrated, and by stopping nephrotoxic agents. The patient should be catheterised to allow monitoring of their urine output. (see 5.4.4)

4. Monitor serum K+ and glucose; the serum K+ is should be monitored closely in all patients with hyperkalaemia to assess efficacy of treatment and to look for rebound hyperkalaemia after the initial response to treatment wanes. Serum potassium be assessed at least 1, 2, 4, 6 and 24 hours after identification and treatment of hyperkalaemia.

Blood glucose concentration should be monitored at regular intervals (0, 15, 30, 60, 90, 120, 180, 240, 300, 360 minutes) for a minimum of 6 hours after administration of insulin-glucose infusion in all patients with hyperkalaemia.

5. Prevent recurrence by identifying and treating the underlying cause(s); this may require referral to the local renal unit (Canterbury for MGH, GSTT for TWH) or the intensive care team for an urgent opinion, and should include a thorough review of the patient, their history and their current medications see (5.4.3).

5.4.2 Administration of calcium salts

Administration of calcium salts calcium chloride or calcium gluconate do not lower the serum potassium but protect the cardiac membrane and should result in improvements (normalisation) of the ECG within 1 to 3 minutes. Both preparations calcium chloride and calcium gluconate, are available in the form of 10ml of 10% solution. Calcium chloride contains approximately three times more calcium (6.8 mmol/ 10ml) as compared with calcium gluconate (2.26mmol/ 10ml). For this reason calcium gluconate may be less efficacious so with calcium gluconate If improvement of the ECG does not occur a further 10ml of 10% calcium gluconate can be given intravenously every 10 minutes until the ECG normalises (patients may require up to 50ml).

The effect of both calcium salts is transient (approximately 30 to 60 minutes), so further doses may be necessary if hyperkalaemia remains uncontrolled.

The main side effects is tissue necrosis if extravasation occurs, other potential adverse effects are peripheral vasodilation, hypotension, bradycardia, syncope and arrhythmia. Calcium gluconate is regarded as less toxic to peripheral veins, however it has been suggested to be less efficacious due to its limited bioavailability because of chelation and the reliance on hepatic metabolism

It is important to note that if the patient is taking digoxin and the decision is made that calcium gluconate is required, it should be given slowly over 20 minutes mixed in 100ml of glucose 5% as rapid calcium administration may precipitate myocardial digoxin toxicity


Digoxin toxicity can itself cause hyperkalaemia and arrhythmias and urgent haemodialysis or the administration of digoxin antibody (Fab) fragments may represent the preferred approach. In this case, consult with senior colleagues

5.4.3 Shift the potassium from the blood into the cell

These interventions buy time for more definitive therapy but do not remove potassium from the body.

Insulin dextrose:

Insulin-glucose infusion (10 units soluble insulin in 50ml of 50% dextrose (25g glucose)) by intravenous infusion over 15-30 minutes into a large vein. This causes potassium concentration to decrease within 15 minutes of starting the infusion, with the peak reduction (of approximately 0.65-1.0 mmol/L) occurring between 30-60 minutes, and lasting approximately 2-6 hours. Potassium levels should be checked hourly during this period of treatment.

The main risk of insulin-glucose therapy is hypoglycaemia. Blood glucose should be measured at 15, 30 and 60 minutes after starting the infusion and then hourly for a minimum of six hours after completion of the infusion (or more regularly if indicated) as delayed hypoglycaemia may occur.

In some circumstances (circulatory shock, diabetic ketoacidosis) capillary glucose testing with a glucometer may not provide an accurate or reliable measure of blood glucose. In these circumstances or if the glucose level measured by capillary testing does not correspond with the clinical picture, a venous blood sample should be sent to the laboratory for analysis. A drop of blood from the venous sample can be tested using the glucometer to assess if a discrepancy exists with the capillary measurement. Comparison of the venous with the laboratory sample will confirm the glucometer is properly calibrated

Salbutamol nebulisers:

The efficacy of insulin-glucose is increased if given in combination with salbutamol.

Tremor, palpitations (increase in heart rate >15 per minute) and headache are the most frequently reported adverse effects. Mild hyperglycaemia has also been reported and this may partly protect against insulin-induced hypoglycaemia.

The effect of salbutamol is dose-dependent, the onset of action is within 30 minutes with peak effect within 60 minutes and lasts for at least 2 hours.

Non-selective beta-blockers may prevent the hypokalaemic response to salbutamol

Salbutamol may not lower potassium in all patients and some studies show that up to 40% of dialysis dependent patients are resistant to these agents. The hypokalaemic response is also attenuated in patients taking digoxin.


Sodium bicarbonate:

Administration of 8.4% sodium bicarbonate is not usually recommended. While this has been a traditional treatment for hyperkalaemia, some studies showed that sodium bicarbonate failed to lower the serum potassium and that any reduction in potassium was delayed (>60 minutes after administration). There are also potential risks in giving sodium bicarbonate in terms of volume and sodium overload and tetany in patients with chronic renal failure and co-existent hypocalcaemia.

The risks are thought to outweigh potential benefit in most cases, but up to 50mls of 8.4% may be administered. In the presence of significant acidosis it may be appropriate to administer 1.26% sodium bicarbonate in aliquots of 250-500ml following the serum bicarbonate and potassium levels.

5.4.4 Remove potassium from the body.

Cation-exchange resins are cross-linked polymers with negatively charged structural units which can exchange bound sodium (Kayexalate) or calcium (calcium resonium) for cations including K+. Their onset of action is slow which limits their use in emergencies.

Evidence in support for the use of cation-exchange resins in the treatment of hyperkalaemia is limited and suggests that multiple doses are required over several days with lowering of serum K+ occuring over 1 to 5 days.

The use of calcium resonium is contraindicated in bowel obstruction. The most serious adverse effect of resins is intestinal necrosis which can occur when they are given orally or as an enema.

Constipation is common; therefore, resins are usually given in combination with a cathartic such as lactulose 15ml twice daily, it is unclear whether the K+ lowering effect is attributable to the resin or induction of diarrhoea.

Oral administration of calcium resonium in adults should be as 15g orally 3-4 times daily. It can be added to syrup or milk for greater palatability. Do not add Calcium Resonium to fruit juice which has a high potassium content. As the onset of action of calcium Resonium is delayed, it should be stopped when the potassium is <5.5mmol/L. Co prescription of a regular laxative (lactulose 15ml) is recommended.

Rectal administration of Calcium resonium is by administration of 30g dissolved in 150 ml of water as an enema. The enema should be retained for at least 9 hours then the colon irrigated to remove resin. Due to the difficulty in ensuring it is retained for the necessary 9 hours and the risk of faecal impaction and bowel perforation that can occur when irrigating the colon to remove resin this method of administration is not recommended. If both routes are used do not continue with rectal administration after oral doses have reached the rectum.

The patients own renal function often remains the most effective route for K+ elimination. Where kidney function has been compromised the cause of this compromise should be identified and treated to optimise the patient’s intrinsic renal function and potassium removal (e.g. correct fluid abnormalities, establish urine output). This should include a review of all the patients normal and recent medications looking for nephrotoxic medications and drugs associated with potassium retention. The patient should be assessed for signs


of dehydration, and if present the patient resuscitated with potassium free intravenous fluids. The patient should also be assessed for signs of renal tract obstruction, and should normally be catheterised to relieve any urinary retention present and to allow hourly monitoring of urine output. An ultrasound of the renal tract will frequently be helpful to ensure that there is no internal obstruction of the renal tract causing hydronephrosis and failure of one or both kidneys.

Renal replacement therapy (RRT) is the most effective and definitive method to treat hyperkalaemia by potassium removal but it is invasive. Urgent referral should be considered If despite initial medical management the potassium remains greater than 7mmol/l or if pathological ECG changes/symptoms persist or if there is ongoing tissue damage and continued release of intracellular potassium is expected.

RRT by continuous veno-venous haemo(dia)filtration can be performed by the critical care units or as haemodialysis by the associated renal units (Canterbury for MGH and Guys for TWH).

5.5 Referral and transfer

Referral to the renal or intensive care team should be guided by the cause of hyperkalaemia, condition of the patient, suitability for treatment, stability for transfer and response to initial medical management. Escalation of care to the critical care unit is not always appropriate. Inappropriate admission to a critical care area may create false hope and unrealistic expectations for patients and their families. It is important to consider factors including aetiology of acute illness, pre-morbid functional status, quality of life and the wishes of the patient. RRT can require insertion of specialist lines and specialist equipment which can take some time, to organise and perform.

If it is appropriate to transfer the patient to one of the associated renal units the safe transfer of the patient should be assured by consideration of the three key steps in optimising patient transfer - firstly, to decide if transfer is absolutely necessary; secondly, to stabilise the patient prior to transfer; and thirdly, to coordinate the transfer itself. Patients should not, in general, be transferred between hospitals if the serum K+ is > or = to 6.5 mmol/L, though other factors will occasionally over-ride this consideration

6.0 Review potentially offending medications

A review of medications to prevent further potassium accumulation should occur identifying potentially offending medications in accordance with the patient’s potassium level and clinical symptoms. These include ACE inhibitors, angiotensin receptor blockers, potassium retaining diuretics e.g. spironolactone, amiloride – (in Frumil®), NSAIDs and K+ containing laxatives (Movicol®, Klean-Prep®, Fybogel®). Betablockers and digoxin should also be reviewed (and withheld if it is safe to do so) as they prevent intracellular buffering of potassium and reduce the effectiveness of insulin-glucose and beta2 agonists.

The patient may need to be started on a low potassium diet. It is imperative that whilst waiting for this diet that the patient does not consume fruit juice, fruits, chocolate, fruit gums, biscuits, coffee or potatoes.


7.0 Post incident checklist

Following management of true hyperkalaemia according to the guidelines above make sure that:

Potassium levels have been rechecked at least 4 hours after the initial measure or as indicated.

Recheck the potassium daily following the incident and periodically thereafter.

Review any medications stopped during the acute episode of hyperkalaemia and restart if appropriate with close monitoring after discussion with a renal physician or senior physician. For example, it may be possible to reintroduce an ACE inhibitor at a lower dose after an isolated incident of acute hyperkalaemia if the patient is given dietary advice.

8.0 Clinical pearls

Always consult the senior doctor responsible for the patient with hyperkalaemia

Always stop food and fluids that exacerbate hyperkalaemia. Review medications that can raise K+ (ACE/ARBs, spironolactone, K+ sparing diuretics, digoxin, NSAIDs) in accordance with the severity of hyperkalaemia and the clinical picture

Careful cardiac monitoring and repeated blood testing including glucose is mandatory

A negative ECG does not negate the need for calcium gluconate and insulin/glucose in severe cases

Digoxin toxicity (probable in renal failure) can increase K+. In such cases, calcium gluconate MUST be administered slowly over 20 minutes mixed in 100ml glucose 5% to prevent myocardial digoxin toxicity. Alternatively, urgent dialysis and administration of digoxin antibody (Fab) fragments could be considered. If in doubt, discuss with senior colleagues and your pharmacist

Insulin can be administered as a single agent without glucose 50%, if patient glucose >15mmol/l

If doubts exist, confirm the accuracy of capillary blood glucose values by using a sample of venous blood for glucometer testing and sending the remainder of the sample to the laboratory for analysis

Beta2 agonists may not lower K+ especially in dialysis patients or those taking beta-blockers or digoxin. Not recommended as a single agent, but may be a useful adjunct where the patient cannot swallow and IV access is difficult

Calcium gluconate/insulin/beta2 agonists are not definitive therapies - they simply buy time for more definitive therapy

Mild hyperkalaemia (K+ <6mmol/L with no ECG changes or clinical symptoms) is common and often well tolerated in patients with chronic renal failure. ACE inhibitors and angiotensin receptor blockers need not be automatically stopped in this patient group provided hyperkalaemia does not become more severe. A low potassium diet should be started and potassium levels rechecked within 2 weeks.


Where a definite cause cannot be established and removed, ensure that the patient is placed on a “low potassium diet” and ban the patient from consuming food with a high potassium content e.g. chocolate, fruit juices, until referred to a dietician

9.0 Monitoring and audit Compliance with the clinical management guideline will be monitored by review by the Resuscitation Committee of periarrest calls and cardiac arrest related to hyperkalaemia.


APPENDIX ONE Process requirements

1.0 Implementation and awareness

Once approved the document will be emailed to the Clinical Governance Assistant for activation on the Trust approved document management database (Q-Pulse) and will be accessible via search on the staff intranet.

Managers should ensure that their staff members are aware of new publications.

2.0 Review

The guideline should be reviewed every two years and updated as required in the light of new evidence and guidelines.

3.0 Archiving

The Trust intranet retains all superseded files in an archive directory in order to maintain document history.


APPENDIX TWO

CONSULTATION ON: Clinical Management Guideline for Acute Hyperkalaemia

Consultation process – Use this form to ensure your consultation has been adequate for the purpose.

Please return comments to: [email protected]_____________

By date: 2nd October 2015

Job title: Date sent dd/mm/yy

Date reply received

Modification suggested?

Y/N

Modification made?

Y/N

The following staff MUST be included in ALL consultations:

Local Counter Fraud Specialist 3/9/15

Clinical Governance Assistant 27/4/16 28/4/16 Y Y

Chief Pharmacist (if pharmacy/prescribing issues are included in the document)

3/9/15

Please list key staff whose reply is compulsory before approval can be granted:

Please list other staff to be included in the consultation but whose reply is not compulsory:

CD Medicine 3/9/15

CD Surgery 3/9/15

CD Anaesthesia 3/9/15

DTC Chair 3/9/15

MD 3/9/15

DN 3/9/15

ED Clinical Lead 3/9/15 4/9/15 Y Y

The following staff have consented for their names to appear in this and any associated documents:

Dr James Wood

The role of those staff being consulted upon as above is to ensure that they have shared the policy for comments with all staff within their sphere of responsibility who would be able to contribute to the development of the policy.


APPENDIX THREE

Equality Impact Assessment

In line with race, disability and gender equalities legislation, public bodies like MTW are required to assess and consult on how their policies and practices affect different groups, and to monitor any possible negative impact on equality. The completion of the following Equality Impact Assessment grid is therefore mandatory and should be undertaken as part of the policy development and approval process.

Title of policy or practice

Clinical Management Guideline for Acute Hyperkalaemia

What are the aims of the policy or practice?

To ensure best practice in the management of hyperkalaemia

Identify the data and research used to assist the analysis and assessment

Literature review and review of guidelines

Analyse and assess the likely impact on equality or potential discrimination with each of the following groups.

Is there an adverse impact or potential discrimination (yes/no). If yes give details.

Males or Females no

People of different ages no

People of different ethnic groups no

People of different religious beliefs no

People who do not speak English as a first language

no

People who have a physical disability no

People who have a mental disability no

Women who are pregnant or on maternity leave

no

Single parent families no

People with different sexual orientations no

People with different work patterns (part time, full time, job share, short term contractors, employed, unemployed)

no

People in deprived areas and people from different socio-economic groups

no

Asylum seekers and refugees no

Prisoners and people confined to closed institutions, community offenders

no

Carers no

If you identified potential discrimination is it minimal and justifiable and therefore does not require a stage 2 assessment?

When will you monitor and review your EqIA?

Alongside this policy/procedure when it is reviewed.

Where do you plan to publish the results of your Equality Impact Assessment?

As Appendix 3 of this policy/procedure on the Trust approved document management database on the intranet, under ‘Trust polices, procedures and leaflets’.

clinical management guideline for acute hyperkalaemia...3-lead ecg monitoring should be initiated...

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