Paediatric Nephrology Date of submission March 2014

Transcription

1 Hyperkalaemia Title of Guideline (must include the word Guideline (not protocol, policy, procedure etc) Contact Name and Job Title (author) Guideline for the assessment and management of hyperkalaemia in paediatric patients David Broodbank ST7 Paediatrics Corinne Langstaff Consultant Paediatric Nephrologist Directorate & Speciality Family Health Paediatric Nephrology Date of submission March 2014 Date on which guideline must be reviewed (this should be one to three years) Explicit definition of patient group to which it applies (e.g. inclusion and exclusion criteria, diagnosis) Abstract Key Words Statement of the evidence base of the guideline has the guideline been peer reviewed by colleagues? Evidence base: (1-5) 1a meta analysis of randomised controlled trials 1b at least one randomised controlled trial 2a at least one well-designed controlled study without randomisation 2b at least one other type of well-designed quasiexperimental study 3 well designed non-experimental descriptive studies (ie comparative / correlation and case studies) 4 expert committee reports or opinions and / or clinical experiences of respected authorities 5 recommended best practise based on the clinical experience of the guideline developer Consultation Process Target audience March 2019 Children and Young People presenting to Nottingham Children s Hospital With Hyperkalaemia This guideline describes the Assessment and Management of Hyperkalaemia in Paediatric patients. Hyperkalaemia, High Potassium, Child, Young Person, Renal, 1a Children s Renal Unit guideline review. Paediatric Clinical Guidelines Group Clinicians and healthcare professionals caring for children and young people treated for Hyperkalaemia at Nottingham University Hospitals NHS Trust This guideline has been registered with the trust. However, clinical guidelines are guidelines only. The interpretation and application of clinical guidelines will remain the responsibility of the individual clinician. If in doubt contact a senior colleague or expert. Caution is advised when using guidelines after the review date. Corinne Longstaff Page 1 of 9 March2014

2 Document Control Document Amendment Record Version Issue Date Author Description V V2 Feb 2014 David Broodbank ST7 Paediatrics Corinne Langstaff Consultant Paediatric Nephrologist General Notes: Summary of changes for new version: This guideline replaces the previous guidance on paediatric hyperkalaemia contained within the Fluid and Electrolyte Management guideline (June 2008). This guideline places more emphasis on the possible causes of hyperkalaemia and has an altered treatment algorithm with drug doses in line with the PICU pharmacopeia. Corinne Longstaff Page 2 of 9 March2014

3 Introduction True hyperkalaemia is a rare but life threatening emergency. The causes are wide ranging but the clinical priority lies in treating the raised potassium and ensuring the stability of the patient followed by investigations to establish the cause. In many incidences the hyperkalaemia may not be true (pseudohyperkalaemia) and in clinical situations where high potassium is unexpected and the patient is well then a repeat of the test may be all that is required. Potassium Physiology Potassium is predominantly an intracellular cation with 98% of the body s potassium within cells. This situation is maintained by the Na + -K + ATPase pump and determines cellular resting potential and hence explains the serious consequences of hyperkalaemia. Total body potassium is governed by dietary intake and excretion by the kidney at the collecting duct under the influence of aldosterone where potassium is exchanged for sodium. Adequate distal tubular delivery of sodium is therefore required to remove potassium, this may not be the case in situations of avid sodium and water retention by the kidney such as dehydration. Normal Ranges Under 2 weeks age mmol/l 2 weeks 3 months mmol/l Over 3 months mmol/l Clinical Features Symptoms are rare but those with severe hyperkalaemia may experience Muscle weakness Palpitations or syncope secondary to cardiac conduction disturbance Corinne Longstaff Page 3 of 9 March2014

4 Causes Pseudohyperkalaemia Haemolysed blood sample Hereditary spherocytosis and familial pseudohyperkalaemia (potassium leaks from cells as a result of cooling) EDTA contamination of sample (take lithium heparin samples first) Hyperventilation e.g. due to crying (acute respiratory alkalosis may cause potassium to shift out of cells) Significant leucocytosis or thrombocytosis Sample taken from arm receiving IV fluids containing potassium Increased Potassium Intake High potassium load from IV fluids or TPN Blood transfusion Drugs containing a large amount of potassium In children with normal renal function and hormonal mechanisms dietary intake should not cause significant hyperkalaemia Movement of potassium from intracellular to extracellular space Cellular Injury o Rhabdomyolysis, trauma, burns o Severe haemolysis o Tumour lysis syndrome Metabolic or respiratory acidosis Hyperkalaemic periodic paralysis Insulin deficiency Drugs e.g. beta blockers, suxamethonium, digoxin toxicity Impaired renal excretion of potassium Chronic or acute kidney disease o The ability to excrete potassium is relatively well maintained until the GFR is <15 ml/min/1.73m 2. However, children with lesser degrees of renal impairment may have other factors. e.g. drugs, or dehydration which enhance the risk of hyperkalaemia Dehydration / hypovolaemia Aldosterone deficiency o Primary adrenal insufficiency o Adrenal enzyme deficiencies Congenital adrenal hyperplasia Aldosterone synthase deficiency Aldosterone resistance o Pseudohypoaldosteronism types 1 and 2 o Secondary type 4 renal tubular acidosis may be associated with sickle cell disease, urinary tract obstruction and/or urinary tract infection Drugs o Potassium sparing diuretics e.g. spironolactone, amiloride o Non-steroidal anti-inflammatory drugs e.g. ibuprofen o ACE inhibitiors e.g. captopril, enalapril, lisinopril o Angiotensin 2 receptor blockers e.g. losartan o Calcineurin inhibitors e.g. ciclosporin, tacrolimus Corinne Longstaff Page 4 of 9 March2014

5 Treatment Flow Chart Stop all potassium enhancing fluids (including blood products) Stop medications which may increase serum potassium (check all medications with pharmacy) Treat underlying cause if known (eg. shock) but consider avoiding / delaying blood products as these contain significant amounts of potassium Mild/Moderate Hyperkalaemia K+ > 5.9 mmol/l Severe Hyperkalaemia K mmol/l Check history -? likely pseudohyperkalaemia Repeat K + on free flowing venous sample Place on a cardiac monitor and confirm hyperkalaemia with blood gas Obtain an ECG (do not let ECG delay treatment) Review medications (including fluids) with pharmacist Review diet (refer to dietitian) Discuss early with paediatric nephrologist on call if evidence of acute kidney injury ECG changes (see appendix 3) Stabilise Cardiac Membrane 0.5mL/kg (max 20mL) Calcium Gluconate 10% IV over 5-10 min. Repeat after 5 min if ECG changes persist No ECG changes Immediate Management Salbutamol 2.5-5mg via nebuliser (repeat as needed) Or IV 4 micrograms/kg over 5 minutes (min. interval between IV doses is 2 hours) Further Management Check potassium 30 mins after intervention Liaise EARLY with paediatric nephrologist (may need dialysis) Consider admission to PICU / HDU Repeat nebulised or IV Salbutamol as above if ongoing hyperkalaemia Consider Sodium bicarbonate if acidotic (see appendix 1 for dosing) do not give if corrected Ca <2.0 mmol/l or ionised Ca < 1.0 mmol/l +/- Consider Furosemide 1mg/kg IV over 5-10 minutes (higher doses may be required in renal failure) (may be given alongside salbutamol) +/- Consider Insulin / Dextrose Infusion (see appendix 1 for dosing) if ongoing hyperkalaemia despite regular salbutamol Ongoing Management (usually in liaison with Pediatric Nephrologist) Regular Furosemide +/- Calcium resonium (or Sodium resonium if hyponatraemic) -see appendices 1 and 2 Dialysis (Especially in CKD / AKI eg. HUS) Dietitian referral Corinne Longstaff Page 5 of 9 March2014

6 References 1)Mahoney BA, Smith WA, LO DS et al. Emergency interventions for hyperkalaemia. Cochrane Database Syst Rev 2005, :CD )Masilamani K, van der Voort J. The management of acute hyperkalaemia in neonates and children. Arch Dis Child 2012; 97:376. 3)Somers JM. Management of hyperkalaemia in children. In: UpToDate, Basow, DS (Ed), UpToDate, Waltham, MA, )Somers JM. Causes, diagnosis and evaluation of hyperkalaemia in children. In: UpToDate, Basow, DS (Ed), UpToDate, Waltham, MA, )Rees L, Brogan P, Bockenhauer D, Webb N. Paediatric Nephrology 2 nd Ed. Oxford University Press )Behrman, Kliegman, Jenson. Nelson Textbook of Pediatrics 17 th Ed. Saunders Corinne Longstaff Page 6 of 9 March2014

7 Appendix 1 Insulin and glucose dosing regime 0.1 units/kg in 5 ml/kg of 20% dextrose, given over 30 minutes. Check blood sugar 15 and 30 minutes after infusion finished. Can be repeated after 1 hour if needed: effect on potassium lasts for approx. 1hr Central route preferred due to glucose strength. Or 0.1 units/kg in 10ml/kg of 10% dextrose, given over 30 minutes. Check blood sugar 15 and 30 minutes after infusion finished. Can be repeated after 1 hour if needed: effect on potassium lasts for approx 1 hour This latter regime may be more appropriate if the infusion needs to be given peripherally due to the glucose strength. However in patients with renal failure who are fluid restricted a clinical judgement will need to be made as to the most appropriate regimen. Sodium Bicarbonate dosing regime 1 mmol/kg as a single dose infused over 30 minutes. The 8.4% solution should ideally be diluted 1 in 5 for central administration and 1 in 10 for peripheral administration. Suitable diluents include 0.9% sodium chloride, 5% glucose and 10% glucose. In arrest or other emergency situations, or in fluid restricted patients, the 4.2% solution can be given NEAT peripherally to patients under 2 years, and the 8.4% solution can be given NEAT peripherally to those over 2 years. However, exercise extreme caution and monitor infusion site closely. NB, check corrected or ionised calcium and treat hypocalcaemia before giving sodium bicarbonate - risk of severe hypocalcaemia and seizures/tetany IV Salbutamol dosing regime 4 microgram/kg as a single dose over 5 minutes. Repeat as necessary. Minimum interval between doses: 2 hours. Dilute to 50micrograms/1ml with 0.9% saline, 5% glucose or water for injection. Draw up required dose and give over 5 minutes. Doses less than 50 micrograms should be further diluted (e.g. to 5ml) prior to administration. Calcium resonium dosing regime Oral: 1 month -18 years mg/kg (max 15 g) 3-4 times daily (may take >24 hours to work and should be given with lactulose to avoid impaction, the hypokalaemic effect may persist so treatment should be stopped when potassium is high normal). Rectal: Birth-18 years mg/kg 3-4 times daily if necessary (irrigate colon to remove resin after 6-12 hours. NB Pre-mixed solution of calcium resonium is available on ward E17 at Queens Medical Centre. See appendix 2 for guide to measuring doses. Corinne Longstaff Page 7 of 9 March2014

8 Appendix 2 A Guide to the Approximate Measurement of Calcium or Sodium Resonium Doses using a 5mL Medicine Spoon. 4g 5g 6g 7g 9g Images from Sherwood Forest Hospitals Pharmacy Dept: acknowledged with thanks. Corinne Longstaff Page 8 of 9 March2014

9 Appendix 3 ECG abnormalities Normal Peaked T waves Wide QRS Wide complex tachycardia Increasing potassium Wide complex tachycardia is due to delayed repolarisation and ventricular fibrillation or asystole may follow. Conduction abnormalities are more common if: the rise in potassium is sudden there are co-existing abnormalities in sodium or calcium the patient is acidotic. Corinne Longstaff Page 9 of 9 March2014