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Management of Hyperkalemia
according to NICE Guidelines
By/Sadek Al-Rokh
 Consultant Acute medicine & Endocrinology and Diabetes
(East Sussex trust UK).
 MRCP (UK).
 SCE Acute medicine of the royal college of physicians .
 SCE Endocrine and diabetes of the royal college of
physicians.
 European board in Endocrine and diabetes.
Grades of hyperkalemia
Mild Hyperkalaemia
5.5 – 5.9 mmol/L  If eGFR has not increased
>10% or no acute increase in K
can repeat in 1-2 weeks.
 Review medications & diet for
causes.
Moderate Hyperkalaemia
6.0- 6.4 mmol/L  Recheck ASAP.
 If ECG changes admit.
 Stop medications that may
elevate K.
Severe Hyperkalaemia
≥6.5 mmol/L or if ECG
changes present
 Urgent repeat: Admit
Causes of Hyperkalemia
 Decreased potassium excretion
 Drug induced:
 Potassium sparing diuretics (Spironolactone, Amiloride, co-amilofruse)
 ACE inhibitor, ARBS, NSAIDs , Beta blockers, Digoxin Excess, Cyclosporine, tacrolimus,
Heparin)
 Renal failure (Acute or chronic).
 Addison disease.
 Type IV renal tubular acidosis.
 Shift of potassium into extracellular space
 Metabolic acidosis (i.e. DKA).
 Rhabdomyolysis , Tumor lysis syndrome ,
 Hemolysis.
Causes of Hyperkalemia
 Increased potassium intake
 High-potassium, low-sodium diets.
 Ingestion of potassium supplement.
 Entral feeding (Glucerna , Ensure).
 PRBC transfusion (risk peaks at 2-3 weeks of cell storage)
 Pseudohyperkalemia(Spurious hyperkalemia)
(Potassium high in blood sample but not in patient):
 Traumatic venipuncture.
 Delay in reaching laboratory.
 Contamination with EDTA (FBC) in tube.
 Haemolysis during venipuncture or excess cuff time.
 Thrombocytosis –Leukocytosis.
Causes of Hyperkalemia
 Genetic disorders
 Congenital adrenal hyperplasia (CAH).
 Pseudohypoaldosteronism.
 Hyperkalemic periodic paralysis (HYPP).
Signs and Symptoms of hyperkalemia
 Neuromuscular symptoms (Muscle weakness and paresthesia).
 Hypotension.
 Syncope (due to arrhythmia).
 ECG changes (Bradycardi and arrthmia as prescribed below ) :
Investigations & Monitoring :
 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.
 Serum creatinine&Urea and Electrolytes for possible AKI or CKD.
 Venous 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 hospital hypoglycemia
management pathway.
Treatment of Severe Hyperkalemia :
 If serum potassium is > 6.5 mmol/L or any
hyperkalaemia is accompanied by ECG changes
or symptoms then seek advice and give urgent
treatment as below :
1-ECG monitoring :
 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.
 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 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).
Treatment of Severe Hyperkalemia
2-Protect cardiac membrane :
 Give 10mL of calcium gluconate 10% intravenously via slow IV bolus into a large peripheral
vein over 10 minutes.
 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.
 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.
 A normal ECG does not negate the need for calcium gluconate or calcium chloride 10%
injection.
 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.
 The effect of this treatment is transient and lasts 30 minutes.
 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).
 Administration of calcium gluconate 10% or calcium chloride 10% injection does not lower
serum potassium therefore other interventions are urgently required.
Treatment of Severe Hyperkalemia
3-Shift potassium from blood into the cells :
 Administer Insulin/glucose infusion.
 Check blood glucose levels first prior to infusing insulin and correct hypoglycaemia
in the patient if present‫ز‬
 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.
 The onset of hypokalaemic action occurs within 15 minutes after the start of the
infusion & lasts around 60 minutes.
 The administration of insulin/glucose infusion can be repeated. Administer up to
three times to lower serum potassium levels.
 Monitor for hypoglycemia and check 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.
 If hypoglycaemia does occur glucose tablets/gel should be used in preference to
orange/fruit juice due to its high potassium content.
 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.
Treatment of Severe Hyperkalemia
4-Administer salbutamol via nebulisation
 Give salbutamol 10mg – 20mg via nebulisation.
 Its effects are seen within 15-30 minutes lasting up to 2 hours.
 Patients with ischemic heart disease should receive the lower dose of
10mg.
 Avoid in patients with significant tachycardia (heart-rate > 120bpm).
 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.
Treatment of Severe Hyperkalemia
5-Stop further potassium accumulation :
 Review & stop all potentially offending drugs or infusions on drug chart.
 Beta-blockers and digoxin should also be reviewed (and witheld temporarily if it safe
to do so) as they reduce the effectiveness of salbutamol nebulizer & insulin-glucose
infusion.
 Place the patient on a low potassium diet.
 Correct underlying cause of hyperkalaemia (i.e. acute kidney injury, sepsis)
6- 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
organize this management plan.
 Hemodialysis is the most effective and definitive method in treating hyperkalaemia by
actually removing potassium from the body but it is invasive.
Treatment of moderate Hyperkalemia :
 If 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:
 A 12-lead ECG – is mandatory for all patients with serum potassium levels >6.0
mmol/L prior to treatment of hyperkalaemia.
 Review and stop all potentially offending drugs or infusions on drug chart.
 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.
 Place the patient on a low potassium diet.
 Correct underlying cause (i.e. acute kidney injury, sepsis).
Treatment of moderate Hyperkalemia :
 Administer Insulin/glucose infusion (Discussed before).
 Administer salbutamol via nebulization (Discussed before).
 Remove potassium from the gut – cation-exchange resins (Calcium polystyrene
sulphonate) resin (Calcium Resonium® ) 15 grams orally 3-4 times daily.
 The powder should be given in a small amount of water.
 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.
 Prescribe with regular lactulose solution 15 mL orally twice daily will help increase gut
losses of potassium and prevent constipation.
 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.
 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.
Treatment of mild Hyperkalaemia :
 If serum potassium is < 6.0 mmol/L AND ECG changes
and symptoms are absent then give the following
treatment for patients:
 Temporarily stop all potentially offending drugs or infusions on drug
chart.
 Put the patient on a low potassium diet.
 Correct underlying cause of hyperkalemia (i.e. acute kidney injury,
sepsis).
 Consider removal of potassium from the gut – cation-exchange
resins (Discussed before).
Post treatment checklist :
 Following management of hyperkalemia 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
hyperkalemia 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 hyperkalemia 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).
Treatment in Cardiac arrest due to hyperkalemia:
 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:
 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.
 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.
 Administer sodium Bicarbonate 50mmol by rapid intravenous bolus via peripheral or central or IO
access.
 Do not give calcium solutions and sodium bicarbonate solutions simultaneously by the same
route.
 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.
 The treatment steps can be repeated according to the clinical condition of the patient and the
results of a repeat blood gas analysis.
 Consider hemodialysis in patients who have suffered a cardiac arrest induced by hyperkalaemia
which is resistant to medical treatment. Contact renal/ITU team urgently for advice.
Treatment of hyperkalemia due to digoxin toxicity
 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.
 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.
Use of Sodium Bicarbonate in treatment of
hyperkalemia
 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.
 Administration of Sodium Bicarbonate 1.26%. Advice from the renal
team must always be sought prior to its use.
Best wishes

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Hyperkalemia

  • 1. Management of Hyperkalemia according to NICE Guidelines By/Sadek Al-Rokh  Consultant Acute medicine & Endocrinology and Diabetes (East Sussex trust UK).  MRCP (UK).  SCE Acute medicine of the royal college of physicians .  SCE Endocrine and diabetes of the royal college of physicians.  European board in Endocrine and diabetes.
  • 2. Grades of hyperkalemia Mild Hyperkalaemia 5.5 – 5.9 mmol/L  If eGFR has not increased >10% or no acute increase in K can repeat in 1-2 weeks.  Review medications & diet for causes. Moderate Hyperkalaemia 6.0- 6.4 mmol/L  Recheck ASAP.  If ECG changes admit.  Stop medications that may elevate K. Severe Hyperkalaemia ≥6.5 mmol/L or if ECG changes present  Urgent repeat: Admit
  • 3. Causes of Hyperkalemia  Decreased potassium excretion  Drug induced:  Potassium sparing diuretics (Spironolactone, Amiloride, co-amilofruse)  ACE inhibitor, ARBS, NSAIDs , Beta blockers, Digoxin Excess, Cyclosporine, tacrolimus, Heparin)  Renal failure (Acute or chronic).  Addison disease.  Type IV renal tubular acidosis.  Shift of potassium into extracellular space  Metabolic acidosis (i.e. DKA).  Rhabdomyolysis , Tumor lysis syndrome ,  Hemolysis.
  • 4. Causes of Hyperkalemia  Increased potassium intake  High-potassium, low-sodium diets.  Ingestion of potassium supplement.  Entral feeding (Glucerna , Ensure).  PRBC transfusion (risk peaks at 2-3 weeks of cell storage)  Pseudohyperkalemia(Spurious hyperkalemia) (Potassium high in blood sample but not in patient):  Traumatic venipuncture.  Delay in reaching laboratory.  Contamination with EDTA (FBC) in tube.  Haemolysis during venipuncture or excess cuff time.  Thrombocytosis –Leukocytosis.
  • 5. Causes of Hyperkalemia  Genetic disorders  Congenital adrenal hyperplasia (CAH).  Pseudohypoaldosteronism.  Hyperkalemic periodic paralysis (HYPP).
  • 6. Signs and Symptoms of hyperkalemia  Neuromuscular symptoms (Muscle weakness and paresthesia).  Hypotension.  Syncope (due to arrhythmia).  ECG changes (Bradycardi and arrthmia as prescribed below ) :
  • 7. Investigations & Monitoring :  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.  Serum creatinine&Urea and Electrolytes for possible AKI or CKD.  Venous 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 hospital hypoglycemia management pathway.
  • 8. Treatment of Severe Hyperkalemia :  If serum potassium is > 6.5 mmol/L or any hyperkalaemia is accompanied by ECG changes or symptoms then seek advice and give urgent treatment as below : 1-ECG monitoring :  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.  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 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).
  • 9. Treatment of Severe Hyperkalemia 2-Protect cardiac membrane :  Give 10mL of calcium gluconate 10% intravenously via slow IV bolus into a large peripheral vein over 10 minutes.  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.  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.  A normal ECG does not negate the need for calcium gluconate or calcium chloride 10% injection.  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.  The effect of this treatment is transient and lasts 30 minutes.  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).  Administration of calcium gluconate 10% or calcium chloride 10% injection does not lower serum potassium therefore other interventions are urgently required.
  • 10. Treatment of Severe Hyperkalemia 3-Shift potassium from blood into the cells :  Administer Insulin/glucose infusion.  Check blood glucose levels first prior to infusing insulin and correct hypoglycaemia in the patient if present‫ز‬  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.  The onset of hypokalaemic action occurs within 15 minutes after the start of the infusion & lasts around 60 minutes.  The administration of insulin/glucose infusion can be repeated. Administer up to three times to lower serum potassium levels.  Monitor for hypoglycemia and check 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.  If hypoglycaemia does occur glucose tablets/gel should be used in preference to orange/fruit juice due to its high potassium content.  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.
  • 11. Treatment of Severe Hyperkalemia 4-Administer salbutamol via nebulisation  Give salbutamol 10mg – 20mg via nebulisation.  Its effects are seen within 15-30 minutes lasting up to 2 hours.  Patients with ischemic heart disease should receive the lower dose of 10mg.  Avoid in patients with significant tachycardia (heart-rate > 120bpm).  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.
  • 12. Treatment of Severe Hyperkalemia 5-Stop further potassium accumulation :  Review & stop all potentially offending drugs or infusions on drug chart.  Beta-blockers and digoxin should also be reviewed (and witheld temporarily if it safe to do so) as they reduce the effectiveness of salbutamol nebulizer & insulin-glucose infusion.  Place the patient on a low potassium diet.  Correct underlying cause of hyperkalaemia (i.e. acute kidney injury, sepsis) 6- 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 organize this management plan.  Hemodialysis is the most effective and definitive method in treating hyperkalaemia by actually removing potassium from the body but it is invasive.
  • 13. Treatment of moderate Hyperkalemia :  If 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:  A 12-lead ECG – is mandatory for all patients with serum potassium levels >6.0 mmol/L prior to treatment of hyperkalaemia.  Review and stop all potentially offending drugs or infusions on drug chart.  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.  Place the patient on a low potassium diet.  Correct underlying cause (i.e. acute kidney injury, sepsis).
  • 14. Treatment of moderate Hyperkalemia :  Administer Insulin/glucose infusion (Discussed before).  Administer salbutamol via nebulization (Discussed before).  Remove potassium from the gut – cation-exchange resins (Calcium polystyrene sulphonate) resin (Calcium Resonium® ) 15 grams orally 3-4 times daily.  The powder should be given in a small amount of water.  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.  Prescribe with regular lactulose solution 15 mL orally twice daily will help increase gut losses of potassium and prevent constipation.  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.  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.
  • 15. Treatment of mild Hyperkalaemia :  If serum potassium is < 6.0 mmol/L AND ECG changes and symptoms are absent then give the following treatment for patients:  Temporarily stop all potentially offending drugs or infusions on drug chart.  Put the patient on a low potassium diet.  Correct underlying cause of hyperkalemia (i.e. acute kidney injury, sepsis).  Consider removal of potassium from the gut – cation-exchange resins (Discussed before).
  • 16. Post treatment checklist :  Following management of hyperkalemia 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 hyperkalemia 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 hyperkalemia 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).
  • 17. Treatment in Cardiac arrest due to hyperkalemia:  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:  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.  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.  Administer sodium Bicarbonate 50mmol by rapid intravenous bolus via peripheral or central or IO access.  Do not give calcium solutions and sodium bicarbonate solutions simultaneously by the same route.  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.  The treatment steps can be repeated according to the clinical condition of the patient and the results of a repeat blood gas analysis.  Consider hemodialysis in patients who have suffered a cardiac arrest induced by hyperkalaemia which is resistant to medical treatment. Contact renal/ITU team urgently for advice.
  • 18. Treatment of hyperkalemia due to digoxin toxicity  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.  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.
  • 19. Use of Sodium Bicarbonate in treatment of hyperkalemia  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.  Administration of Sodium Bicarbonate 1.26%. Advice from the renal team must always be sought prior to its use.