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|Neonates||K+ > 6.0mmol/L|
|Child and adult||K+ > 5.5mmo/L|
Patients with chronic kidney disease (CKD) and low GFR (less than 30) may have persistent or recurrent hyperkalemia and may be tolerant of higher levels of potassium than those with sudden onset hyperkalemia. For CKD patients with potassium of 5.5 - 6.5 mmol/L, discuss promptly with the paediatric nephrologist on call.
Capillary blood collections will increase haemolysis of cells and increase serum potassium. To exclude the effect of haemolysis, an elevated serum potassium collected by capillary method must be repeated with a running venous blood specimen. Pseudo-hyperkalemia can also be seen in disorders with extremely high white or red cell counts
- Large packed red cell transfusions
- Medications - high dose penicillin G
- Errors in IV KCl dose calculation
- Liquid formulas and foods (salt substitutes)
- Excessive cellular damage from trauma, burns
Transcellular K+ shift
- Insulin deficiency (NB: fasting in renal failure patients)
- Hyperosmolarity (mannitol)
- Non specific β2 Blockers due to blocking of catecholamine induced uptake
- ACE inhibitors (ACEI), Angiotensin Receptor Blockers (ARBs), aldosterone antagonists
- Succinylcholine (in burns, cord injury, trauma patients).
Reduced renal excretion
- Renal failure
- Inherited or acquired tubular dysfunction
- Mineralocorticoid deficiency
- Drug effect - spironolactone, NSAIDs. ACEI and ARBs, trimethoprim
Investigations for Chronic Hyperkalemia
- Complete serum biochemistry including creatinine, urea, blood gas
- Urine potassium
- Other investigations if chronic hyperkalemia considered - first morning plasma renin, aldosterone, urine electrolytes (K+, osmolality, creatinine)
- Calculate Transtubular K gradient (TTKG) -
TTKG = Urine K x Urine Osmolality
Plasma K Plasma Osmolality
TTKG <7 in presence of hyperkalemia suggests impaired excretion due to deficiency or resistance to mineralocorticoid (this is not accurate if urine is more dilute than serum or contains very little Na+
- Recognise acute adrenal insufficiency due to abrupt cessation of steroids ( treat with hydrocortisone, volume replacement)
- Start continuous ECG monitoring
- Stop all medications, and IV fluids that may contain potassium
- Assess cardiac effects with urgent ECG (12 lead) when K+ > 6.0-6.5mmol/L
- If ECG changes of hyperkalemia are present treat immediately - see below.
- Potassium lowering measures
- Potassium shifting therapies - sodium bicarbonate, salbutamol, insulin & dextrose
- Potassium removing therapies - resonium, acute dialysis
ECG Changes Of Hyperkalemia
Narrow peaked T waves, U waves, shortened QT interval, prolonged
PR interval, prolonged QRS interval, loss of P wave, sine waves and
finally ventricular fibrillation (see ECG guideline
for normal values for age)
ECG CHANGES DO NOT NECESSARILY PROGRESS IN ORDER OF SERIOUSNESS OR SEVERITY, IN RELATION TO THE SEVERITY OF HYPERKALEMIA.
Hyperkalemia with severe ECG changes (not isolated peaked T waves) is a Medical Emergency
- Notify PICU.
- Give IV calcium gluconate urgently if there is widening of QRS complex or loss of P waves. In this situation, a registrar can administer IV calcium gluconate through a large peripheral fasting running vein such as in the antecubital fossa.
- Nebulised salbutamol can be started while IV dextrose and insulin is set up.
Hyperkalemia without ECG changes must still be treated urgently with nebulised salbutamol which can be started while IV dextrose and insulin is set up.
Medications in Hyperkalemia
|Calcium gluconate 10%1||Stabilises membrane
|Immediate / 30min||0.5mls/kg (max 20ml)|
|Salbutamol2,3||K+ shift intracellularly||20min / 2-4hrs||2.5-5mg neb|
|Insulin4||K+ shift intracellularly||20min / 4-6hrs||If have central IV access
0.1u/kg actrapid iv bolus plus 2mls/kg 50% dextrose iv bolus
No central IV access
0.1u/kg iv bolus plus
5 mls/kg 10% dextrose iv bolus
In both cases check dextrose stick at 15 and 30 minutes
|Resonium5,6||Removes K by exchange across colon||1-2hrs / 4-6hrs||1gm/kg PR|
|Frusemide7||Inhibits K reabsorption in Nephron||10min||1-2mg/kg IV stat|
- Hyperkalemia with severe ECG changes (not isolated peaked T waves) is a medical emergency (see above).
- Salbutamol is the treatment of first choice because of ease of administration while other treatments are being set up.
- Salbutamol and IV insulin have additive effect. The magnitude of potassium lowering effect is unpredictable and not all patients will benefit. These are only short term treatments while definitive treatment is being organised
- Insulin and β2 adrenergic receptors stimulate Na-K+ ATPase pump activity
- Sodium resonium contains a large amount of sodium and can result in volume overload
- Resonium has its effect principally through potassium exchange
in colon, therefore rectal administration is preferred. If there
are specific contraindications to rectal use (e.g. after large
bowel surgery or suspected bowel obstruction) then oral
administration is acceptable.
Coagulopathy should not be a contraindication unless they have active rectal bleeding, e.g. in patients with GVHD or severe mucositis.
SORBITOL should NOT be used to make up resonium mixture as it has been associated with colonic necrosis
Neonates should not be given resonium due to reduced gut motility
- Frusemide is only effective if renal function is relatively normal.
Frank Shann. Drug Doses 15th edition 2010. RCH publications
Kamel KS, Wei C. Controversial issues in the treatment of hyperkalemia. Nephrol Dial Transpl 2003;18:2215-2218
Kiessling SG, Goebel J, Somers MJG. Pediatric Nephrology in the ICU. 2009. Springer
Did you find this information helpful?
- Date last published: 01 February 2017
- Document type: Clinical Guideline
- Services responsible: Paediatric Nephrology, Paediatric Intensive Care Unit
- Author(s): William Wong, Gabrielle Nuthall
- Editor: Greg Williams
- Review frequency: 2 years
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