21.3 Electrolyte Disorders: Sodium, Potassium, Calcium, Magnesium and Phosphate
Key Takeaways
Severe symptomatic hyponatraemia (seizures, coma) is treated with 150 mL of 3% saline over about 20 minutes, repeated as needed, aiming for a rise of about 5 mmol/L; the total correction should not exceed about 10 mmol/L in the first 24 hours to avoid osmotic demyelination.
Hyperkalaemia with ECG changes is treated first with intravenous calcium to stabilise the myocardium, then insulin with glucose and nebulised salbutamol to shift potassium into cells, and finally removal by binders or dialysis.
Hypokalaemia causes U waves, flattened T waves and arrhythmias; intravenous potassium is usually given at no more than 10-20 mmol/h peripherally, with higher rates only through a central line with ECG monitoring.
Magnesium sulphate 2 g intravenously is the treatment for torsades de pointes, and low magnesium makes hypokalaemia resistant to correction.
Hypocalcaemia after parathyroidectomy, thyroidectomy or massive transfusion causes perioral tingling, tetany, Chvostek's and Trousseau's signs, and QT prolongation; treat symptomatic cases with intravenous calcium gluconate.
21.3 Electrolyte Disorders: Sodium, Potassium, Calcium, Magnesium and Phosphate
Sodium and Water
Plasma sodium reflects the balance between sodium and water: most disorders are disorders of water handling. Normal plasma sodium is about 135-145 mmol/L, and plasma osmolality about 275-295 mOsm/kg, estimated as (all in mmol/L).
Hyponatraemia (Below 135 mmol/L)
Assessment:
- Confirm hypotonic hyponatraemia (measured osmolality low); exclude hyperglycaemia (translocational) and pseudohyponatraemia (severe hyperlipidaemia or paraproteinaemia with older analysers).
- Assess volume status and measure urine osmolality and urine sodium.
| Volume status | Urine sodium | Causes |
|---|---|---|
| Hypovolaemic | Below 30 mmol/L | Vomiting, diarrhoea, burns, third-space losses |
| Hypovolaemic | Above 30 mmol/L | Diuretics (especially thiazides), adrenal insufficiency, cerebral salt wasting |
| Euvolaemic | Above 30 mmol/L | SIADH, hypothyroidism, glucocorticoid deficiency |
| Hypervolaemic | Usually below 30 mmol/L | Heart failure, cirrhosis, nephrotic syndrome |
Perioperative causes: hypotonic fluids with non-osmotic ADH release, transurethral resection syndrome (absorption of glycine irrigation fluid), thiazides, SSRIs and carbamazepine.
Clinical features: nausea, headache, confusion, seizures, coma and cerebral oedema, especially when the fall is acute (under 48 hours). Premenopausal women and children are at greater risk of encephalopathy.
Treatment (European guidance, 2014):
- Severe symptoms (vomiting, seizures, reduced consciousness): 150 mL of 3% saline over 20 minutes, check sodium, and repeat up to two or three times until sodium has risen by about 5 mmol/L.
- Limit the total rise to 10 mmol/L in the first 24 hours and 8 mmol/L in each subsequent 24 hours, because rapid correction of chronic hyponatraemia causes osmotic demyelination syndrome (dysarthria, dysphagia, quadriparesis). Lower limits (for example 8 mmol/L in 24 hours) are used for patients at high risk, such as those with alcoholism or malnutrition.
- Chronic asymptomatic: treat the cause; fluid restriction for SIADH; stop offending drugs.
- If correction is too rapid, re-lowering with 5% glucose and desmopressin can be considered.
Hypernatraemia (Above 145 mmol/L)
Usually caused by water loss without adequate intake (fever, diarrhoea, osmotic diuresis), diabetes insipidus (cranial after head injury or pituitary surgery, or nephrogenic with lithium), or iatrogenic sodium loading (hypertonic saline, sodium bicarbonate).
- Diabetes insipidus: large volumes of dilute urine (osmolality below about 300 mOsm/kg) with rising plasma sodium; cranial DI responds to desmopressin.
- Correction: replace water deficit gradually (enterally or with 5% glucose), aiming for a fall of no more than about 10-12 mmol/L per day in chronic hypernatraemia to avoid cerebral oedema.
Potassium
Normal plasma potassium is about 3.5-5.3 mmol/L; about 98% of total body potassium is intracellular. Insulin, beta-2 agonists and alkalosis move potassium into cells; acidosis, cell damage and hyperosmolality move it out.
Hypokalaemia
- Causes: diuretics, vomiting, diarrhoea, insulin, beta-2 agonists, alkalosis, hypomagnesaemia, Conn's syndrome, refeeding.
- Features: weakness, ileus, arrhythmias, potentiation of digoxin toxicity; ECG shows flattened T waves, ST depression, U waves and a prolonged QU interval.
- Treatment: oral replacement when possible; intravenous potassium chloride is usually given at no more than 10-20 mmol/h through a peripheral vein (concentration limits apply). Faster rates (up to about 40 mmol/h) need a central line and continuous ECG monitoring in a critical care setting. Correct magnesium at the same time.
Hyperkalaemia
- Causes: renal failure, potassium-sparing diuretics, ACE inhibitors and angiotensin receptor blockers, acidosis, rhabdomyolysis, tumour lysis, reperfusion, massive transfusion of old blood, suxamethonium in susceptible patients, adrenal insufficiency.
- Pseudohyperkalaemia: haemolysed samples, high platelet or white cell counts.
- ECG progression: peaked T waves, then prolonged PR and flattened P waves, then widening QRS, sine-wave pattern, ventricular fibrillation or asystole.
Emergency treatment:
1. PROTECT THE HEART: calcium chloride 10% 10 mL or calcium gluconate 10% 30 mL IV
(works within minutes, lasts 30-60 min; repeat if ECG changes persist)
2. SHIFT POTASSIUM INTO CELLS:
- Insulin 10 units with 25 g glucose IV (falls by about 0.6-1.0 mmol/L in 30-60 min)
- Nebulised salbutamol 10-20 mg (additive)
- Sodium bicarbonate if acidotic
3. REMOVE POTASSIUM: binders (sodium zirconium cyclosilicate, patiromer),
loop diuretics, haemodialysis for refractory cases
4. Monitor glucose (hypoglycaemia risk) and potassium
Calcium
About 45% of plasma calcium is ionised (the active fraction, about 1.1-1.3 mmol/L), 45% is protein-bound (mainly albumin) and 10% is complexed. Total calcium is about 2.2-2.6 mmol/L. Alkalosis increases protein binding and lowers ionised calcium.
Hypocalcaemia
- Causes: hypoparathyroidism (after thyroid or parathyroid surgery), vitamin D deficiency, pancreatitis, rhabdomyolysis, citrate from massive transfusion, hypomagnesaemia, sepsis.
- Features: perioral and peripheral paraesthesia, muscle cramps, tetany, laryngospasm, seizures, hypotension, QT prolongation; Chvostek's sign (facial twitching when tapping the facial nerve) and Trousseau's sign (carpal spasm with an inflated blood pressure cuff).
- Treatment: symptomatic or severe: calcium gluconate 10% 10-20 mL intravenously over about 10 minutes, then an infusion; calcium chloride delivers about three times as much elemental calcium per mL but is more irritant and is best given centrally. Correct magnesium.
Hypercalcaemia
- Causes: primary hyperparathyroidism and malignancy account for about 90%; also thiazides, sarcoidosis, immobilisation.
- Features: "bones, stones, abdominal groans and psychic moans": polyuria, dehydration, constipation, confusion, renal stones, short QT.
- Treatment: intravenous saline rehydration, then bisphosphonates (zoledronic acid) for malignancy; calcitonin acts quickly but briefly; treat the cause.
Magnesium
Normal plasma magnesium is about 0.7-1.0 mmol/L. Magnesium is a cofactor for Na/K-ATPase and a physiological calcium antagonist.
- Hypomagnesaemia: diuretics, alcoholism, diarrhoea, proton pump inhibitors, refeeding. Causes arrhythmias (including torsades de pointes), tetany, seizures and refractory hypokalaemia and hypocalcaemia.
- Treatment: magnesium sulphate 2 g (8 mmol) intravenously over about 10-20 minutes; for torsades de pointes, 2 g over a few minutes.
- Hypermagnesaemia: renal failure or magnesium therapy (for example pre-eclampsia). Loss of tendon reflexes (about 4-5 mmol/L), respiratory depression and heart block at higher levels; potentiates neuromuscular blockers. Treat with intravenous calcium and stop the infusion.
Phosphate
Normal plasma phosphate is about 0.8-1.5 mmol/L. Phosphate is needed for ATP and 2,3-diphosphoglycerate.
- Hypophosphataemia: refeeding syndrome, alcohol withdrawal, diabetic ketoacidosis treatment, respiratory alkalosis, renal replacement therapy. Severe deficiency (below about 0.3 mmol/L) causes respiratory muscle weakness (failure to wean), cardiac dysfunction, haemolysis and rhabdomyolysis. Replace intravenously in severe cases.
- Hyperphosphataemia: renal failure, rhabdomyolysis, tumour lysis; causes hypocalcaemia and metastatic calcification.
A patient develops a sodium of 118 mmol/L with a generalised seizure 6 hours after transurethral resection of the prostate with glycine irrigation. What is the immediate treatment?
Fluid restriction to 1 litre per day and repeat sodium in 24 hours
Intravenous 0.9% saline at 2 litres per hour until the sodium concentration is normal
150 mL of 3% saline over 20 minutes, repeated to raise sodium by about 5 mmol/L
Desmopressin 2 micrograms intravenously
A patient's potassium is 7.4 mmol/L with broad QRS complexes. What is the first drug to give?
Insulin 10 units with 25 g glucose, because it lowers potassium fastest
Intravenous calcium to stabilise the myocardium
An oral potassium binder, because it removes potassium from the body
Furosemide 40 mg intravenously
After total thyroidectomy, a patient reports perioral tingling, and carpal spasm occurs when a blood pressure cuff is inflated. Ionised calcium is 0.78 mmol/L. Which treatment and ECG finding are expected?
Intravenous calcium gluconate; the ECG may show QT prolongation
Intravenous saline and zoledronic acid; the ECG shows a short QT interval
Oral phosphate supplements; the ECG shows peaked T waves
Magnesium restriction; the ECG shows U waves
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