Paeds · nephrology-urology-fluids-and-electrolytes
Hypokalaemia and hyperkalaemia
Also known as Hypokalaemia · Hyperkalaemia · Potassium disorders · Dyskalaemia · Low potassium · High potassium · Potassium emergency
Fellowship guide to potassium disorders in children: hypokalaemia as a serum potassium below 3.5 and hyperkalaemia as above 5.5 mmol/L, the three-axis classification of intake, transcellular shift and renal or gut loss, the cardiac membrane electrophysiology behind peaked T waves and U waves, emergency management of hyperkalaemia with calcium gluconate, salbutamol and insulin-dextrose, safe intravenous potassium replacement for hypokalaemia, Bartter and Gitelman syndromes, and hypomagnesaemia as the cause of refractory hypokalaemia.
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- Any child with hyperkalaemia and ECG changes — peaked T waves, widened QRS, or a sine wave — needs intravenous calcium gluconate now to stabilise the myocardium; do not wait for a repeat potassium, because the next beat can be asystole
- Severe hypokalaemia below 2.5 mmol/L with muscle weakness, paralysis, ileus, or U waves is an emergency that needs controlled intravenous potassium chloride at a maximum of 0.2 mmol/kg/hour peripherally with cardiac monitoring — never an undiluted bolus
- Hypokalaemia that will not correct is hypomagnesaemia until proven otherwise — low magnesium disinhibits ROMK and drives renal potassium loss, so the potassium will not be retained until magnesium is replaced
- A high serum potassium in diabetic ketoacidosis is misleading — total-body potassium is always depleted, and insulin will drive it down precipitously within hours, so anticipate the fall and have potassium ready
- A normal-looking ECG does not exclude dangerous hyperkalaemia — the ECG is an imperfect predictor, so treat the level when it is severe even if the tracing looks benign
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- Definition of hypokalaemia and hyperkalaemia by serum potassium
- Three axes of potassium balance: intake, shift, loss
- ECG changes of hyperkalaemia and the calcium-first rule
- Bartter versus Gitelman syndrome: the calcium and magnesium tie-breaker
- Safe intravenous potassium replacement and the rate limit
- Insulin-dextrose, salbutamol and hypoglycaemia risk in hyperkalaemia
- Emergency management of severe hyperkalaemia with ECG changes
- Hypomagnesaemia as the cause of refractory hypokalaemia
- The potassium arm of diabetic ketoacidosis
- Short case: a child with weakness and U waves
- Long case: an adolescent with Gitelman syndrome
- Communication station explaining safe potassium replacement to a family
- Nephrology and fluids: disorders of potassium balance
- Investigation and emergency management of hyperkalaemia
- Inherited hypokalaemic tubulopathies
- Physiology of potassium homeostasis and the resting membrane potential
- Classification of dyskalaemia and the ECG signatures
- Pharmacology of calcium gluconate, salbutamol, insulin-dextrose and potassium chloride
- Clinical assessment and ECG interpretation in the dyskalaemic child
- Communication: explaining hyperkalaemia treatment to a family
- Hypokalaemia and hyperkalaemia: definition, causes and emergency management
- ECG changes and the calcium-gluconate-first rule
- Bartter and Gitelman syndromes
- Patient Care: potassium disorders and cardiac monitoring
- Medical Knowledge: cellular potassium physiology and pharmacology
- Systems-Based Practice: safe intravenous potassium protocols
- Nephrology: potassium homeostasis and dyskalaemia
- Emergency management of hyperkalaemia in children
- Inherited tubulopathies: Bartter and Gitelman syndromes
Potassium is the dominant intracellular cation: about 98 percent of the body's store sits inside cells, and only a sliver lives in the small extracellular compartment the serum measures. This single fact explains almost everything about potassium disease. A child can lose hundreds of millimoles from the body and still show a near-normal serum level, because insulin, catecholamines and acid-base status keep shifting potassium back and forth across the cell membrane to defend that level. It also explains why a small shift out of cells — a little acidosis, a dose of digoxin, a fast-growing tumour breaking down — can move the serum potassium into the danger zone long before total-body potassium is high. [4] [1]
This page treats the two disorders as a mirror image. Hyperkalaemia is the faster killer — it stops the heart — so it gets the resuscitation framework: calcium, salbutamol, insulin-dextrose, removal. Hypokalaemia is the quieter danger — it weakens muscle and prolongs repolarisation — so it gets the replacement framework: oral versus intravenous, the rate limit, and magnesium. Both share the same organising logic: classify by the three axes, let the ECG set the tempo, and treat the cause while you treat the number. [1] [3]
Overview & Definition
Hypokalaemia is a serum potassium below 3.5 mmol/L. It is graded as mild (3.0 to 3.5), moderate (2.5 to 3.0) and severe (below 2.5); severe disease, or any level with symptoms or ECG changes, is an emergency. Hyperkalaemia is a serum potassium above 5.5 mmol/L. In newborn upper bound is slightly higher, but any level above 6.5 mmol/L, or any level with ECG changes at all, is a true emergency. Both thresholds are serum values, and both demand a repeat sample to exclude artefact before you act on an asymptomatic, mildly abnormal result. [1] [4]
The serum potassium is a concentration, not a content. It tells you how much potassium sits in the extracellular water at that instant, not how much the whole body holds. A child in diabetic ketoacidosis may walk in with a serum potassium of 5.0 mmol/L and a total-body deficit of 3 to 6 mmol/kg, because the acidosis has shifted intracellular potassium out into the blood while the urine has been washing it away for days. The number and the deficit point in opposite directions, and this is the trap that catches the unwary prescriber. [4] [3]
References11ShowHide
- [1]Zieg J; Ghose S; Raina R Electrolyte disorders related emergencies in children. BMC Nephrol, 2024.PMID 39215244
- [2]Rubens M; Kanaris C Fifteen-minute consultation: Emergency management of children presenting with hyperkalaemia. Arch Dis Child Educ Pract Ed, 2022.PMID 34344762
- [3]Masilamani K; van der Voort J The management of acute hyperkalaemia in neonates and children. Arch Dis Child, 2012.PMID 21920871
- [4]Viera AJ; Wouk N Potassium Disorders: Hypokalemia and Hyperkalemia. Am Fam Physician, 2015.PMID 26371733
- [5]Kemper MJ; Harps E; Hellwege HH; Müller-Wiefel DE Effective treatment of acute hyperkalaemia in childhood by short-term infusion of salbutamol. Eur J Pediatr, 1996.PMID 8789768
- [6]McClure RJ; Prasad VK; Brocklebank JT Treatment of hyperkalaemia using intravenous and nebulised salbutamol. Arch Dis Child, 1994.PMID 8129434
- [7]Moussavi K; Fitter S; Gabrielson SW; Koyfman A Management of Hyperkalemia With Insulin and Glucose: Pearls for the Emergency Clinician. J Emerg Med, 2019.PMID 31084947
- [8]Crnobrnja L; Metlapalli M; Jiang C; Govinna M The Association of Insulin-dextrose Treatment with Hypoglycemia in Patients with Hyperkalemia. Sci Rep, 2020.PMID 33328554
- [9]Fulchiero R; Seo-Mayer P Bartter Syndrome and Gitelman Syndrome. Pediatr Clin North Am, 2019.PMID 30454738
- [10]Blanchard A; Bockenhauer D; Bolignano D; Calò LA Gitelman syndrome: consensus and guidance from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference. Kidney Int, 2017.PMID 28003083
- [11]Assadi F; Mazaheri M; Rad EM Electrocardiography is Unreliable to Detect Potential Lethal Hyperkalemia in Patients with Non-dialysis Chronic Kidney Disease. Pediatr Cardiol, 2022.PMID 35389084