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GUIDELINE FOR THE MANAGEMENT OF HYPERKALAEMIA IN ADULTS
This guidance does not override the individual responsibility of health professionals to make appropriate decision according to the circumstances of the individual patient in consultation with the patient and /or carer. Health care professionals must be prepared to justify any deviation from this guidance.
Introduction This guideline is to provide education and guidance to prescribers and healthcare professionals involved in treating adult patients with hyperkalaemia. The guideline outlines the management and treatment of adult patients with proven hyperkalaemia reported on a laboratory blood sample (WAHT reference range for potassium is: 3.5 – 5.3 mmol/L). The guideline is based on the latest national hyperkalaemia management guidelines produced by GAIN in 2008 (Guidelines and Audit Implementation Network) accessed via: http://www.gain-ni.org/Publications/Guidelines/hyperkalaemia guidelines.pdf and the UK Renal Association July 2012 accessed via: www.renal.org/guidelines in May 2013.
This guideline is for use by the following staff groups : All qualified healthcare professionals involved in the care and management of adult patients with hyperkalaemia.
Lead Clinician(s) Dr Martin Ferring Consultant Renal Medicine, WRH
Dr Stephen Spencer Consultant Renal Medicine, WRH
Approved by Clinical Management Committee on: 20 th November 2013
Approved by Medicines Safety Committee on: 15th October 2013
Extension approved by TMC on: 22nd July 2015
This guideline should not be used after end of: 20th November 2017
Key amendments to this guideline Date Amendment By: October 2013 New guideline February 2015 Document extended for 12 months as per TMC paper TMC approved on 22nd July 2015 December Further 12 months extension to document TMC 2016
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GUIDELINE FOR THE MANAGEMENT OF HYPERKALAEMIA IN ADULTS
Introduction
The incidence of hyperkalaemia in hospitalised patients is between 1-10%. The majority of cases are drug-induced in the patient in conjunction with pre-existing or newly diagnosed renal failure. Hyperkalaemia should be regarded as a medical emergency as it can be life- threatening. A precipitating medication should be considered for all patients presenting with hyperkalaemia and promptly discontinued. Severe hyperkalaemia requires urgent treatment, but needs to be distinguished from spurious hyperkalaemia (high in blood sample but not in patient). To be effective, medications for the treatment of hyperkalaemia need to be given correctly; to be safe, they require appropriate monitoring, so as to avoid serious complications such as hypoglycaemic coma after insulin-glucose administration. This guideline outlines a standardised approach to the treatment of hyperkalaemia in adults to minimise the potential risks associated with its management.
Causes There can be several different causes of hyperkalaemia, including:
Renal failure - including Acute kidney injury (AKI), advanced chronic kidney disease (CKD) stages 4 & 5 or renal tubular acidosis (type IV). Spurious hyperkalaemia: o Sample taken from a limb infused with IV fluids containing potassium. o Wrong sequence of blood collection i.e. EDTA (purple top) sample for FBC collected before serum tube (gold type). o Cell lysis – potassium release from cells (tumour lysis syndrome, rhabdomyolysis, trauma, burns) o High platelet count and high white blood cell counts – can artificially raise serum potassium. o Prolonged tourniquet time. o Haemolysed samples due to difficult collection or delayed transport to lab of more than 4 hours. o In all cases a repeat serum potassium should be ordered urgently. Metabolic acidosis (transcellular shift of K+ from intracellular to extracellular compartments) Drugs – see below Addison’s disease – and other adrenal insufficiency /resistance states including hypoadrenalism.
Drug-induced hyperkalaemia: This is not an exhaustive list. Contact your ward Pharmacist or Medicines Information (ext: 30235) for more advice. If essential drug(s) are the underlying cause and need discontinuing please contact relevant specialities/senior staff for advice and to check if alternative drug(s) are required; ACE-inhibitors (e.g. ramipril, lisinopril, perindopril) Angiotensin II receptor blockers (e.g. candesartan, losartan, olmesartan) Spironolactone & other potassium sparing diuretics (e.g. co-amilofruse, amiloride) Potassium supplements (Sando K®, Slow K® tablets, Kay-Cee-L® syrup) Intravenous fluids containing potassium (e.g. Hartmanns) Aliskiren (Direct renin inhibitor)
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Less common causative drugs: NSAIDs (it it safe to continue low dose aspirin 75mg or 150mg daily) Potassium containing laxatives (Movicol® or Laxido®, Klean-prep®) Beta-blockers – may increase transcellular shift of K+ to extracellular compartments Digoxin – in toxicity states hyperkalaemia & arrhythmias can result Heparins (rarely) Trimethoprim
Classification Of Hyperkalaemia
WAHT reference range for serum potassium: 3.5 – 5.3mmol/L
Severity of hyperkalaemia: Severe Moderate Mild K ≥ 6.5 mmol/L K 6.1 to 6.4 mmol/L AND K ≤ 6 mmol/L AND OR ECG normal AND ECG normal AND ECG changes* present with a No symptoms No symptoms present K+ >5.5mmol/l OR Neuromuscular symptoms Spurious hyperkalaemia? (potassium high in blood sample but not in patient)
(*) ECG changes of life-threatening hyperkalaemia:
Absent P-waves Prolonged PR QRS widening / sine wave QRST Heart block Cardiac arrest (Tented T-waves alone are NOT life-threatening and not treated routinely)
Signs And Symptoms
Patients may be asymptomatic but hyperkalaemia can cause: ECG changes (as above) Syncope (due to arrhythmia) Neuromuscular symptoms (paraesthesia) PRESENCE OF THESE SYMPTOMS INDICATE SEVERE Muscle weakness HYPERKALAEMIA & URGENT Hypotension TREATMENT IS NEEDED Bradycardia
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Initial Clinical Assessment
It is recommended all patients with suspected or confirmed hyperkalaemia undergo the following: Urgent assessment by medical & Nursing staff to assess clinical status using the ABCDE approach (Ref: appendix II page 9). A detailed history & examination – to determine cause of raised potassium. A review of their drug history, prescription chart, Intravenous fluid chart or enteral feeds for potential potassium promoting drugs or infusions (Ref: list page 3). Seek advice from a Pharmacist as soon as possible.
THE CAUSE FOR HYPERKALAEMIA MUST BE SEARCHED FOR AND TREATED URGENTLY.
An appropriate escalation plan should be put in place for the patient taking into account their symptoms may include arrhythmias.
Investigations & Monitoring
Repeat urea & electrolytes (U & Es) – mark ‘URGENT’ & inform Lab. If out of hours telephone lab to inform them of urgent request to ensure it is processed as a quickly as possible. Repeating serum potassium urgently is necessary to exclude spurious hyperkalaemia, especially if hyperkalaemia is unexpected or an isolated finding and there are no ECG changes in the patient. Review serum creatinine for possible AKI or CKD. Arterial blood gas sample. Serum potassium levels may be assessed on an arterial or venous blood sample using a point of care blood-gas analyser in emergencies whilst awaiting a formal laboratory result. Monitor U &Es and venous bicarbonate – for possible Acidosis (e.g. renal failure, renal tubular acidosis, hypocortisolism). Continue to monitor serum potassium and response to treatment or possible potassium rebound by rechecking U & Es: - 1 hour after treatment commenced - At least every 6 hours until potassium within normal range Conduct a 12-lead ECG – this is mandatory for all patients with raised serum potassium levels prior to treatment of hyperkalaemia. Note the ECG may not demonstrate changes even in the presence of severe hyperkalaemia. Monitor blood glucose levels to exclude hypoglycaemia prior to commencing treatment. If hypoglycaemia is present treat according to trust’s hypoglycaemia management pathway (Ref: Hypoglycaemia management WAHT- END-004).
Referral
Ask for immediate ITU input or advice from the renal team for all SEVERE hyperkalaemia cases. Discuss with the renal team any patients with asymptomatic hyperkalaemia <6.5 mmol/L if serum potassium levels are not normalising in the patient following treatment.
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Treatment Overview
Remember the majority of treatments discussed below including calcium gluconate injection, calcium chloride injection, insulin/glucose infusion and salbutamol nebules only work short- term and may need repeating to be effective. These treatment options may be sufficient if the underlying cause for hyperkalaemia is treated quickly (i.e. stopping an offending drug or siting a catheter to relieve bladder obstruction and resolve AKI).These treatment options alone will not be sufficient if the underlying cause for hyperkalaemia cannot be corrected (i.e. in a dialysis patient with no kidney function) or in cases where there is a rapid rise in potassium production (i.e. tumour lysis or rhabdomyolysis). Dialysis removes potassium from the body and is the most effective and definitive method in treating hyperkalaemia but this is an invasive treatment option. Patients already receiving dialysis in community will normally require this treatment option urgently if they are admitted into hospital with hyperkalemia (ref: point 5).
Table 1: Treatment Overview
MANAGEMENT TREATMENT SEVERE MODERATE MILD NOTES Calcium YES NO-unless NO - unless Calcium chloride 10% should only GLUCONATE ECG ECG be administered if central access is injection 10% 10mls changes changes available (never give peripherally) present or present or (Ref: points 2.1 – 2.9). (or Calcium patient patient If patients are prescribed digoxin CHLORIDE injection symptomatic symptomatic infuse calcium gluconate 10% 10mL 10% 10mL) in 100mls glucose 5% slowly over 20 minutes (ref: point 2.7) Insulin/glucose Yes YES-if NO Administration instructions refer to infusion deemed a points 3.1.1-3.1.8. suitable Risk of hypoglycaemia. Monitor blood treatment by glucose levels prior to commencing their clinician infusion to exclude hypoglycaemia. Follow trust’s hypoglycaemia management pathway (ref: WAHT- END-004) if hypoglycaemia is present before starting infusion. Salbutamol via Yes YES-if NO Avoid in patients with significant nebulisation deemed a tachycardia (heart-rate>120bpm) due suitable to salbutamol causing increased HR. treatment by Always prescribe with their clinician insulin/dextrose due to additive effects in lowering serum potassium. Stop further YES YES YES Place patient on low potassium diet. potassium Review all medications, infusions & accumulation enteral feeds. Contact Pharmacy for advice. Calcium Resonium® YES-if YES YES-if Slow onset of action (>2 hours). powder deemed a deemed a Prescribe with lactulose 15mL orally suitable suitable twice daily to prevent constipation. treatment by treatment by C/I in obstructive bowel disease & their clinician their clinician hypercalcaemia (ref: point 10.1-10.8).
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Haemodialysis *CONSULT *CONSULT *CONSULT Dialysis is usually required for RENAL/ITU RENAL/ITU RENAL/ITU dialysis patients with hyperkalaemia TEAMS TEAMS TEAMS OR patients not on dialysis with FIRST FIRST FIRST severe/symptomatic hyperkalaemia. Please refer IMMEDIATELY to the renal team/ITU. Sodium bicarbonate *ALWAYS *ALWAYS *ALWAYS The potential risks in administering infusion CONSULT CONSULT CONSULT sodium bicarbonate infusion usually RENAL RENAL RENAL outweigh the benefits. Always contact TEAM FIRST TEAM FIRST TEAM FIRST renal team/Consultants first.
Treatment Of Severe Hyperkalaemia
If serum potassium is > 6.5 mmol/L or hyperkalaemia is accompanied by ECG changes or symptoms then seek advice and give urgent treatment as below
1. ECG monitoring
1.1. A 12-lead ECG is mandatory in patients with severe hyperkalaemia. The ECG does not always demonstrate changes even in the presence of severe hyperkalaemia so a normal ECG does not exclude the need for urgent treatment. 1.2. Patients with a serum potassium >6.5 mmol/L or features of hyperkalaemia on a 12- lead ECG should receive continuous monitoring with a minimum of a 3-lead ECG. 1.3. Patients with a serum potassium of 6.1 – 6.4 mmol/L who are clinically unwell or where a rapid rise of serum potassium is anticipated should also receive continuous monitoring via a 3-lead ECG (preferably in a high care setting).
2. Protect cardiac membrane
2.1. Give 10mL of calcium gluconate 10% intravenously via slow IV bolus into a large peripheral vein over 3-5 minutes. 2.2. If central venous access is available 10mL of calcium chloride 10% administered slowly via a central line over 3-5 minutes is first-line treatment option due to its greater efficacy. Note: this injection must not be administered peripherally due to the potential for venous irritation and tissue necrosis from extravasation. 2.3. These treatments do not lower serum potassium but if ECG changes are present there should be an improvement seen in the ECG within 1-3 minutes. 2.4. A normal ECG does not negate the need for calcium gluconate or calcium chloride 10% injection. 2.5. A further 10mL of calcium gluconate 10% or calcium chloride 10% (central venous access only) should be administered IV every 10 minutes if no improvement is seen initially until the ECG normalises, up to a total of 50mL can be administered. 2.6. The effect of this treatment is transient and lasts 30 minutes. 2.7. If patients are on digoxin 10mL of calcium gluconate 10% injection should be mixed with 100mL of glucose 5% and administered slowly intravenously over 20 minutes. (Rapid calcium administration can precipitate myocardial digoxin toxicity). 2.8. Avoid in patients with hypercalcaemia and seek further advice. 2.9. Administration of calcium gluconate 10% or calcium chloride 10% injection does not lower serum potassium therefore other interventions are urgently required.
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3. Shift potassium from blood into the cells
3.1. Administer Insulin/glucose infusion
3.1.1. Check blood glucose levels first prior to infusing insulin and correct hypoglycaemia in the patient if present (Ref: Hypoglycaemia management WAHT- END-004). 3.1.2. Add 10 units of soluble insulin (Actrapid®) to 50mL of glucose 50%. Infuse over 15 minutes intravenously via an infusion pump. This can be administered peripherally, ideally into a large vein. 3.1.3. Always use a U-100 insulin syringe to measure insulin and obtain a volume and preparation check from a colleague before proceeding. 3.1.4. The onset of hypokalaemic action occurs within 15 minutes after the start of the infusion & lasts around 60 minutes. The reduction in serum potassium ranges from 0.6 – 1.0 mmol/L. 3.1.5. The administration of insulin/glucose infusion can be repeated. Administer up to three times to lower serum potassium levels. 3.1.6. Monitor blood glucose levels 30 minutes after commencing infusion, followed by hourly checks up to 6 hours after the infusion has finished as delayed hypoglycaemia can occur. Monitor patient for symptoms of hypoglycaemia. 3.1.7. Hypoglycaemia should be managed in accordance with trust guidance (Ref: Hypoglycaemia management WAHT-END-004). If hypoglycaemia does occur glucose tablets/gel should be used in preference to orange/fruit juice due to its high potassium content. 3.1.8. Check Urea & electrolytes 30 minutes after each insulin/glucose infusion. If there is a good response U & Es can be checked 1-2 hours later after the last infusion.
3.2. Administer salbutamol via nebulisation
3.2.1. Give salbutamol 10mg – 20mg via nebulisation (unlicensed indication). Its effects are seen within 15-30 minutes lasting up to 2 hours. 3.2.2. Patients with ischaemic heart disease should receive the lower dose of 10mg. 3.2.3. Avoid in patients with significant tachycardia (heart-rate > 120bpm). 3.2.4. The nebuliser chamber will hold 10mL i.e. 10mg at a time. 3.2.5. Salbutamol should never be used as monotherapy for the treatment of severe hyperkalaemia as some patients may not respond to this treatment.
Treatment using a) and b) in patients has additive effects in lowering serum potassium levels so should always be prescribed together for best results.
4. Stop further potassium accumulation
4.1. Review & stop all potentially offending drugs or infusions on drug chart & intravenous prescription chart. 4.2. Beta-blockers and digoxin should also be reviewed (and witheld temporarily if it safe to do so) as they reduce the effectiveness of salbutamol nebules & insulin-glucose infusion. 4.3. Place the patient on a low potassium diet. 4.4. Correct underlying cause of hyperkalaemia (i.e. acute kidney injury, sepsis).
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5. Haemodialysis
If serum potassium levels remain high in a patient (>7 mmol/L) despite the administration of first-line measures above or ECG changes/symptoms persist the renal team should be contacted to arrange urgent dialysis as appropriate. Early referral to the renal team/ITU for advice and management is vital to allow time to organise this management plan. Haemodialysis is the most effective and definitive method in treating hyperkalaemia by actually removing potassium from the body but it is invasive. It is usually required for dialysis patients who are admitted into hospital with hyperkalaemia. It should also be considered if 1st-line treatment options have been unsuccessful in patients with severe hyperkalaemia (>7.0 mmol/L) or where there is a risk of cardiac arrest.
6. Cardiac arrest and hyperkalaemia In patients presumed to be in cardiac arrest secondary to hyperkalaemia use a blood gas analyser to rapidly confirm a diagnosis of hyperkalaemia. Administer treatment to protect the cardiac membrane first followed by the administration of treatments to shift potassium from the blood to inside the cells (Ref: points 2.1 - 3.2.5). Follow the standard advanced life support (ALS) algorithm including basic life support (chest compressions & ventilation). The following treatment steps are recommended by the Resuscitation Council UK:
6.1. Administer 10 mL of calcium chloride 10% by rapid Intravenous bolus via peripheral or central or intraosseous (IO) access. In cardiac arrest only calcium chloride 10% is permitted to be administered via a rapid intravenous bolus peripherally. 6.2. Administer sodium Bicarbonate 50mmol by rapid intravenous bolus via peripheral or central or IO access. 6.3. Do not give calcium solutions and sodium bicarbonate solutions simultaneously by the same route. 6.4. Administer insulin/glucose infusion: Add 10units of soluble insulin (Actrapid®) to 50mL of glucose 50% and administer by rapid intravenous injection via peripheral or central or IO access. Rapid administration of insulin/glucose infusion for the treatment of hyperkalaemia is only permitted in patients who have suffered a cardiac arrest. 6.5. The treatment steps can be repeated according to the clinical condition of the patient and the results of a repeat blood gas analysis. 6.6. Consider haemodialysis in patients who have suffered a cardiac arrest induced by hyperkalaemia which is resistant to medical treatment. Contact renal/ITU team urgently for advice.
7. Further treatment options
7.1. Digoxin toxicity in a patient (especially in renal failure) can lead to hyperkalaemia & arrhythmias. Serum digoxin levels should be checked and monitored in patients with suspected digoxin toxicity and the offending drug discontinued. 7.2. The administration of digoxin-specific antibody fragments (Digifab®) may represent the preferred approach of treatment of a patient. Consult with senior colleagues and seek advice from Pharmacy. 7.3. Administration of Sodium Bicarbonate 1.26%. Advice from the renal team must always be sought prior to its use. An infusion of sodium bicarbonate is usually not recommended. Whilst this has been a traditional treatment option for hyperkalaemia, studies have shown there are potential risks in giving a sodium bicarbonate infusion in terms of volume and sodium overload and tetany in patients with chronic renal failure and co-existing hypocalcaemia. The risks are thought to outweigh potential benefit in most cases. However, in the presence of significant metabolic acidosis (Bicarbonate < 15 mmol/L) it may be appropriate to administer sodium bicarbonate
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1.26% 250 mL-500 mL whilst monitoring the serum concentrations of bicarbonate and potassium levels carefully. 7.4. Remove potassium from the gut. The slow onset of action (>2hours) of cation- exchange resins (Calcium Resonium® powder) makes it unsuitable for the emergency treatment of hyperkalaemia but it could be considered a useful adjunct treatment in these patients (Ref: points 10.1-10.8).
Treatment Of Mild-Moderate Hyperkalaemia
I f serum potassium is 6.0 to 6.4 mmol/L AND ECG changes and symptoms are absent then give the following treatment for patients with non-severe hyperkalaemia: 8. Stop further potassium accumulation
8.1. Review and stop all potentially offending drugs or infusions on drug chart & intravenous prescription chart. 8.2. Beta-blockers and digoxin should also be reviewed (and witheld temporarily if it safe to do so) as they reduce the effectiveness of salbutamol nebules & insulin-glucose infusion. 8.3. Place the patient on a low potassium diet. 8.4. Correct underlying cause (i.e. acute kidney injury, sepsis)
9. Shift potassium from blood into the cells
9.1. Administer Insulin/glucose infusion
9.1.1. Patients with moderate hyperkalaemia (serum potassium levels of 6.0 – 6.4 mmol/L) should receive treatment with an insulin/glucose infusion if deemed appropriate by their Clinician (Ref: points 3.1.1 – 3.1.8).
9.2. Administer salbutamol via nebulisation
9.2.1. Patients with moderate hyperkalaemia (serum potassium levels of 6.0 – 6.4 mmol/L) should receive adjuvant treatment with nebulised salbutamol 10mg- 20mg if deemed appropriate by their Clinician (Ref: 3.2.1 – 3.2.5).
10. Remove potassium from the gut – cation-exchange resins
10.1. Administer Calcium polystyrene sulphonate resin (Calcium Resonium®) 15 grams orally 3-4 times daily. 10.2. The powder should be given in a small amount of water (not fruit juice/squash which has a high potassium content) or made into a paste with a sweetened vehicle i.e. syrup in the ratio of 3 to 4 mL per gram of resin. 10.3. The onset of action is slow (>2 hours) and therefore cation-exchange resins do not have a role in the emergency treatment of patients with severe hyperkalaemia. 10.4. Prescribe with regular lactulose solution 15 mL orally twice daily will help increase gut losses of potassium and prevent constipation. 10.5. Each 1 gram of Calcium Resonium® removes approximately 1 mmol/L of potassium from the gut. 10.6. If the oral route is unavailable, calcium resonium 30 grams can be administered rectally as an enema. The solution must be retained for 9 hours followed by irrigation of the colon to remove resin and prevent faecal impaction. This long
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retention time must be adhered to for successful treatment. Reported complications include bowel perforation and this method of administration must be reserved for patients where other treatment options are unsuitable (Ref: appendix III for further details of administration). Please discuss with a Pharmacist prior to prescribing. 10.7. Administration of Calcium Resonium® orally or rectally is contraindicated in: - Patients with obstructive bowel disease, - Conditions associated with hypercalcaemia, - Patients with serum potassium levels <5.0 mmol/L. 10.8. Potassium levels should be checked at least daily whilst on this treatment and treatment should be discontinued once serum potassium levels are 5.0mmol/l or below as the resin has a prolonged action time and continues to work after administration has stopped.
11. Consider other treatments
Dialysis may need to be considered for some patients (i.e. patients previously on dialysis or with acute kidney injury and poor urine output <0.5 ml/kg /hour). Discuss with renal team &/or ITU.
If serum potassium is < 6.0 mmol/L AND ECG changes and symptoms are absent then give the following treatment for patients:
12. Stop further potassium accumulation
12.1. Temporarily stop all potentially offending drugs or infusions on drug chart & intravenous prescription chart. 12.2. Place the patient on a low potassium diet. 12.3. Correct underlying cause of hyperkalaemia (i.e. acute kidney injury, sepsis)
13. Consider removal of potassium from the gut – cation-exchange resins 13.1. (Ref: 10.1 – 10.8)
Further Information Drugs administered for the treatment of hyperkalaemia must be prescribed on the inpatient prescription administration chart. Remember the term ‘units’ must not be abbreviated when prescribing insulin.
POST TREATMENT CHECKLIST
Following management of hyperkalaemia according to the above guidelines:
Recheck serum potassium levels daily during the patient’s admission and periodically thereafter. Review any medication(s) stopped during an acute episode of hyperkalaemia and restart if necessary with close monitoring. For example it may be necessary to restart a patient’s ACE-inhibitor which could be reintroduced at a lower dose after an isolated case of hyperkalaemia secondary to AKI. Digoxin may need to be recommenced and a lower dose could be recommenced with close serum monitoring in the patient. Contact Pharmacy for advice. Provide the patient with dietary advice on maintaining low potassium intake if needed (i.e. patient’s with CRF).
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Monitoring Tool Via Audit: To be monitored every three years as part of the Trust’s multi-disciplinary Medicines Management Audit Programme:
STANDARDS % CLINICAL EXCEPTIONS Life threatening hyperkalaemia 100% None was managed appropriately as in steps above Management of severe 100% Patients with hypercalcaemia. hyperkalaemia included administration of calcium gluconate 10% injection Management of severe 100% Patients with untreated hyperkalaemia included hypoglycaemia. administration of insulin- glucose infusion. Management of severe 100% Patients with contraindications hyperkalaemia included to nebulised salbutamol. administration of nebulised salbutamol. Blood glucose levels 100% None monitored appropriately after insulin-glucose administration Pseudohyperkalaemia was not 100% Serum potassium >7mmol/l on treated inappropriately initial blood sample.
REFERENCES Guidelines & Audit Implementation Network (GAIN) (2008). Guidelines for the treatment of hyperkalaemia in adults. Accessed via: www.gain-ni.org in May 2013. Alfonzo.A et al (2012). Clinical Practice Guidelines; Treatment of acute hyperkalaemia in adults. UK Renal Association July 2012. Accessed via: www.renal.org/guidelines in May 2013. Summary of Product Characteristics (SPC). Calcium Gluconate Injection BP. Last updated 09/08/10. Accessed via: www.emc.medicines.org.uk in May 2013. Summary of Product Characteristics (SPC). Calcium Resonium®. Last updated 07/07/11. Accessed via: www.emc.medicines.org.uk in May 2013. The British Medical Association & The Royal Pharmaceutical Society of Great Britain (2012). British National Formulary, Number 64: September 2012. The Bath Press, Bath. Injectable Medicines Guideline (Calcium Gluconate injection, Published: 24/11/10) (Accessed on: 08/05/13). Available from: www.injguide.nhs.uk. Injectable Medicines Guideline (Calcium chloride injection, Published: 07/03/11) (Accessed on: 08/05/13). Available from: www.injguide.nhs.uk. King’s College Hospital NHS Foundation Trust (KCHNFT) (2012). Clinical Management Guideline for Hyperkalaemia: Treatment of elevated potassium. Version 1, January 2012. Resuscitation Council (UK) (2011). Advanced Life Support. Sixth Edition. Resuscitation Council (UK). Accessed via: www.resus.org.uk/pages/als.pdf in August 2013.
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Appendix 1 HYPERKALAEMIA TREATMENT FLOWCHART
SEVERE MODERATE MILD K+ > 6.5 mmol/L K+ 6.1 to 6.4 mmol/L K+ <6.0 mmol/L
OR ECG changes present with a and ECG normal and ECG normal K+ >5.5 mmol/ L OR and No symptoms present and No symptoms present Neuromuscular symptoms
Stop all K+ promoting Stop all K+ promoting drugs/infusions and/or K+ drugs/infusions and/or K+ Stop all K+ promoting supplements. drugs/infusions and/or K+ supplements. Check prescription charts & IV fluid Check prescription charts & supplements. charts for k+ promoting drugs. IV fluid charts for k+ Check prescription charts Place patient on a low promoting drugs. & IV fluid charts for k+ potassium diet. promoting drugs.
Place patient on a low Give 10 mL of calcium gluconate potassium diet
10% intravenously via slow IV bolus Correct underlying cause of into a large peripheral vein over 3- hyperkalaemia. Place patient on a low 5 minutes . potassium diet. Use 10 mL of Calcium chloride 10% Correct underlying cause if central access is available. Add 10 units of soluble of hyperkalaemia A further 10 mL of calcium ® insulin (Actrapid ) to 50 mL gluconate 10% (or calcium chloride of 50% glucose and if central access) should be administer over 15 minutes administered IV every 10mins if no Repeat serum potassium via an infusion pump. improvement is seen initially until levels in patients with non- the ECG normalises, up to a total of Monitor blood glucose levels severe hyperkalaemia.
50 mL can be administered. 30 minutes after commencing infusion, followed by hourly checks Consider administering Add 10 units of soluble insulin up to 6 hours after the ® ® Calcium Resonium (Actrapid ) to 50 mL of 50% infusion has finished as powder 15 g orally three- glucose and administer over 15 delayed hypoglycaemia can four times daily minutes via an infusion pump. occur. Co-prescribe Lactulose Monitor blood glucose levels 30 Up to three repeated solution 15 mL orally twice minutes after commencing administrations can be used. infusion, followed by hourly daily to increase gut checks up to 6 hours after the losses & prevent infusion has finished as delayed Give salbutamol 10mg – constipation hypoglycaemia can occur. 20mg via nebulisation. Stop treatment once Up to three repeated serum K+ <5.0 mmol/L administrations can be used. Administer Calcium ® Repeat urea & electrolytes Give salbutamol 10mg – 20mg Resonium powder 15 g in patient following orally three-four times daily via nebulisation . discontinuation of Co-prescribe Lactulose treatment solution 15mL orally twice Haemodialysis – If serum daily to increase gut losses potassium levels remain high in a & prevent constipation patient (>7 mmol/L) despite the Stop treatment once serum administration of first-line measures K+ <5.0 mmol/L above or ECG changes persist the renal team should be contacted to Repeat U & Es following arrange urgent dialysis (ref: point 5) discontinuation of treatment.
All patients with hyperkalaemia should have an urgent clinical assessment using the ABCDE approach (Ref: appendix II) conducted by medical or nursing staff.
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A 12-lead ECG – is mandatory for all patients with serum potassium levels >6.0 mmol/L prior to treatment of hyperkalaemia. Patients with a serum potassium >6.5 mmol/L or features of hyperkalaemia on a 12-lead ECG should receive continuous monitoring with a minimum of a 3-lead ECG. Patients with a serum K+ of 6.1 – 6.4 mmol/L who clinically unwell or where a rapid rise of serum K+ is anticipated should also receive continuous monitoring via a 3-lead ECG
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Appendix 2
ABCDE APPROACH
A – Airway – Recognise and treat airway obstruction.
B – Breathing – Assess adequacy of ventilation: clinical examination, respiratory rate, O2 saturation, arterial blood gas. Give oxygen aiming for ‘normal’ oxygen saturation and provide ventilatory support if necessary.
C – Circulation – Assess cardiovascular status: colour, pulse, BP, volume status, peripheral circulation, urine output (check for palpable bladder), cardiac rhythm (ECG, cardiac monitor), electrolytes (Urea and electrolytes, Mg2+, Ca2+, Phosphate). Establish intravenous access, take bloods. Consider fluid bolus (with care), vasopressors, inotropes treatment of arrhythmia, correct electrolyte abnormalities.
D – Disability - Assess neurological function: AVPU or GCS score and blood glucose - support ABC and correct underlying cause.
E – Exposure – Head to toe assessment and look for evidence of cause, e.g. signs of injuries, compartment syndrome, palpable bladder, skin rashes, dialysis access (central venous catheter, AV fistula, peritoneal dialysis catheter). Check temperature – do not let patient get cold and maintain patient’s dignity at all times.
The ABCDE approach to assess and treat the deteriorating patient.
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Appendix 3
Recommended method of administration for rectal calcium polystyrene sulphonate (Calcium Resonium)
Indication:
Rectal calcium polystyrene sulphonate is used as part of the treatment for hyperkalaemia when patients are unable to take the preparation orally. Calcium polystyrene sulphonate should not be given via enteral feeding tubes as it will block the tubes.
Dose:
The adult dose is 30 g PR retained for 9 hours. It can be used daily.
Equipment needed for administration:
Calcium polystyrene sulphonate powder
Methylcellulose 1% 150mL [available from pharmacy] warmed to body temperature.
Tap water warmed to body temperature.
Rectal catheter or wide bore urethral catheter
Lubricating Jelly.
Bladder syringe.
Method of administration:
1. Administer a warm (body temperature) tap water enema (250-500mL) to remove any faeces in the rectum or sigmoid colon. Please note if there are faeces present in the bowel it may be necessary to affect a rectal lavage. This should be supported by a medical instruction. Refer to the Marsden Manual for the procedure.
2. Add the measured dose of calcium polystyrene sulphonate powder to the warmed methylcellulose solution and shake well until the preparation is of a smooth consistency.
3. Lubricate the nozzle of the catheter with lubricating jelly and introduce the tube into the rectum to a depth of around 10-12.5 cm.
4. Remove the plunger from a bladder syringe and attach to the catheter.
5. Pour the reconstituted calcium polystyrene sulphonate into the syringe and allow it to flow into the patient by gravity.
6. Rinse the bottle with 50-100mL tap water warmed to body temperature and administer via same bladder syringe by gravity.
7. Patient should remain supine with the foot of the bed raised or with pillows placed to elevate the hips as the enema should be retained for 9 hours or as long as possible.
8. After 9 hours, the colon should be irrigated with tap water warmed to body temperature to remove the remaining resin as per the Marsden Manual procedure for rectal lavage.
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References:
McEvoy G, editor. AHFS Drug Information 2009 [Internet]. Bethesda, USA: American Society of Health-System Pharmacists Inc; 2009. [accessed 19.03.10] Available from: www.medicinescomplete.com Sanofi-aventis. Summary of Product Characteristics [Internet]. Calcium Resonium. 27/05/2009. [accessed 19.03.10] Available from: www.emc.medicines.org.uk. Personal communication – Sanofi-aventis 19.03.10. Gloucestershire Royal Hospital Procedure – from MI-UK MailTalk 2006. Sherwood Forest Hospitals Procedure – from MI-UK MailTalk 2002. Marsden Manual http://intranet/WAHT_Library/Marsden_Manual_2004.
(Information provided by Worcestershire Acute Hospitals NHS Trust Medicines Information 22.03.10 R.Fletcher).
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CONTRIBUTION LIST
Key individuals involved in developing the document Name Designation Dr Martin Ferring Consultant Renal Medicine Dr Stephen Spencer Consultant Renal Medicine Joanne Shuck Specialist Clinical Pharmacist, Renal & Endocrinology
Circulated to the following individuals for comments Name Designation Chandrashekar Shetty Consultant Chemical Pathologist Dr David Jenkins Consultant Diabetologist Dr James France Consultant, Emergency Medicine Dr Karen Tait Consultant Diabetologist Rachael Leese Lead Pharmacist, Diabetes AH Keith Hinton Lead Pharmacist, Critical care, Theatres & Surgery Dr Paul Newrick Consultant Diabetologist Tina Evans Clinical Pharmacist, Team Leader Dr Irfan Babar Consultant Diabetologist Rachael Montgomery Chief Pharmacist, Clinical services Dr Simon Hellier Consultant, Gastroenterology Dr David Aldulami Consultant, Medicine Dr Tony Scriven Consultant Cardiologist Dr Miguel Marimon Consultant, Medicine
Circulated to the following CD’s/Heads of dept for comments from their directorates / departments Name Directorate / Department Nick Hubbard Director of Pharmacy Department Ann Carey Head of Nursing Emergency Care
Circulated to the chair of the following committee’s / groups for comments Name Committee / group Nick Hubbard Medicines Safety Committee Alison Smith Principal Pharmacist, Medicines Safety
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Supporting Document 1 - Equality Impact Assessment Tool
To be completed by the key document author and attached to key document when submitted to the appropriate committee for consideration and approval.
Yes/No Comments
1. Does the policy/guidance affect one group less or more favourably than another on the basis of:
Race No
Ethnic origins (including gypsies and No travellers)
Nationality No
Gender No
Culture No
Religion or belief No
Sexual orientation including lesbian, No gay and bisexual people
Age No
2. Is there any evidence that some groups are No affected differently? 3. If you have identified potential N/A discrimination, are any exceptions valid, legal and/or justifiable? 4. Is the impact of the policy/guidance likely to No be negative? 5. If so can the impact be avoided? N/A 6. What alternatives are there to achieving the N/A policy/guidance without the impact? 7. Can we reduce the impact by taking N/A different action?
If you have identified a potential discriminatory impact of this key document, please refer it to Human Resources, together with any suggestions as to the action required to avoid/reduce this impact.
For advice in respect of answering the above questions, please contact Human Resources
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Supporting Document 2 – Financial Impact Assessment
To be completed by the key document author and attached to key document when submitted to the appropriate committee for consideration and approval.
Yes/No Title of document:
1. Does the implementation of this document require any additional No Capital resources 2. Does the implementation of this document require additional No revenue
3. Does the implementation of this document require additional No manpower
4. Does the implementation of this document release any No manpower costs through a change in practice 5. Are there additional staff training costs associated with No implementing this document which cannot be delivered through current training programmes or allocated training times for staff
Other comments:
If the response to any of the above is yes, please complete a business case and which is signed by your Finance Manager and Directorate Manager for consideration by the Accountable Director before progressing to the relevant committee for approval
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