Hypokalaemia and hyperkalaemia — formative SAQs

SAQ 1 (10)

A 7-year-old boy with acute kidney injury secondary to post-infectious glomerulonephritis is noted to have a serum potassium of 7.2 mmol/L. The cardiac monitor shows bradycardia with a widened QRS and tall peaked T waves. He is drowsy but maintains his airway. [2][3]

1. Define hyperkalaemia and explain why this child requires immediate treatment, citing the ECG findings. (2) [2][4]
2. Give the emergency management in the first 30 minutes, naming each drug, dose, route, and its specific purpose, including the monitoring required. (6) [2][7]
3. Outline the definitive steps once he is stabilised, including the role of dialysis, and state two safety pitfalls in this management. (2) [1][8]

Model answer

Definition and urgency. Hyperkalaemia is a serum potassium above 5.5 mmol/L, and this child's level of 7.2 mmol/L is severe and immediately dangerous. The ECG shows bradycardia, a widened QRS and tall peaked (tented) T waves — advanced hyperkalaemic cardiotoxicity that can progress within minutes to a sine wave and asystole. The ECG, not the number alone, mandates emergency treatment now; a repeat result should not delay therapy. [2][4]

Emergency management (first 30 minutes). First, stabilise the myocardium with intravenous 10 percent calcium gluconate 0.5 mL/kg (maximum about 10 mL) given slowly over 5 minutes with continuous cardiac monitoring; this raises the membrane threshold and restores conduction within minutes but does not lower potassium. Second, shift potassium into cells: give nebulised salbutamol 5 mg (he is over 25 kg only if heavier than 25 kg — at a typical 7-year-old weight use 2.5 mg if under 25 kg) together with intravenous insulin 0.1 unit/kg and glucose 0.5 g/kg (for example 5 mL/kg of 10 percent dextrose), which begins to lower potassium within 15 minutes. Third, attach cardiac monitoring and a reliable intravenous line, check blood glucose every 15 to 30 minutes for at least two hours to detect insulin-induced hypoglycaemia, and repeat the potassium at 30 to 60 minutes. [2][7]

Definitive steps and pitfalls. Once stabilised, remove potassium from the body: in a child with acute kidney injury and a refractory or recurring level, the definitive removal is dialysis. Identify and treat the precipitant (the post-infectious glomerulonephritis and any potassium-raising drugs), and restrict potassium intake. Two pitfalls: (1) iatrogenic hypoglycaemia after insulin-dextrose occurs in roughly 10 to 20 percent of treatments and can be severe, prevented only by generous glucose and relentless monitoring; (2) cation-exchange resins are too slow for emergency use and must not be relied on as sole therapy. [1][8]

SAQ 2 (10)

A 14-year-old girl presents with leg cramps and tetany. Her serum potassium is 2.7 mmol/L, bicarbonate 34 mmol/L, blood pressure 105/65 mmHg, and she has a low urinary calcium and a serum magnesium of 0.45 mmol/L. She has had similar episodes for two years. [9][4]

1. What is the most likely diagnosis, and how is it distinguished biochemically from Bartter syndrome? (3) [9]
2. Give the immediate and long-term management of her electrolyte disorder, including the drug doses and the role of magnesium. (5) [4][9]
3. Explain why her hypokalaemia may have been refractory, and outline the surveillance and transition plan. (2) [9]

Model answer

Diagnosis and distinction. This is Gitelman syndrome, a defect of the distal convoluted tubule that mimics a thiazide diuretic. The hallmarks are hypokalaemic metabolic alkalosis with normal-to-low blood pressure, a low urinary calcium, and hypomagnesaemia, presenting later (adolescence) with tetany. Bartter syndrome, a thick ascending limb defect mimicking a loop diuretic, presents earlier (often antenatally or in infancy) and shows hypercalciuria with a risk of nephrocalcinosis. The calcium direction is the tie-breaker: Gitelman is hypocalciuria, Bartter is hypercalciuria. [9]

Management. Immediate management is oral potassium chloride 1 to 2 mmol/kg/day in divided doses together with magnesium replacement (magnesium sulfate or oxide) titrated to correct and maintain serum magnesium, because potassium will not be retained while magnesium is low. Long-term management adds a potassium-sparing diuretic such as amiloride or spironolactone to blunt distal potassium loss and, where symptoms persist, lifelong oral magnesium and potassium supplementation. Intravenous potassium is reserved for severe symptomatic disease, at a maximum of 0.2 mmol/kg/hour peripherally with monitoring. [4][9]

Refractory cause and surveillance. Her hypokalaemia has likely been refractory because the concurrent hypomagnesaemia disinhibits the ROMK channel in the distal nephron, driving continued renal potassium wasting; correcting magnesium is therefore the key to retaining potassium. Surveillance includes serial potassium, magnesium, calcium, renal function and blood pressure, monitoring of growth and bone density, and (in Bartter, not Gitelman) renal ultrasound for nephrocalcinosis. A structured transition to adult nephrology care is part of the plan, with particular attention to magnesium during any future pregnancy. [9]