Electrolyte Replacement Therapy

Electrolyte replacement therapy restores potassium, magnesium, calcium and phosphate when stores or serum levels are low. Most deficits come from gut or kidney losses, poor intake, refeeding, or drugs such as diuretics. The aim is to correct the deficit and the cause, at a speed that avoids harm.

Concentration, rate and route matter as much as dose, because several of these ions cause arrhythmia or tissue injury when given too fast.

Mechanism. Each ion has a narrow working range across cell membranes. Potassium sets resting membrane potential. Magnesium is a cofactor for the sodium-potassium pump and for potassium retention in cells. Calcium drives muscle and nerve excitability and clotting. Phosphate supports energy transfer and bone mineral.

Pharmacokinetics. Oral salts are absorbed in the gut, but some (magnesium, phosphate) cause diarrhoea that limits dose. Intravenous replacement redistributes slowly into cells, so serum levels may rise and then fall back. Kidneys excrete the surplus, so impaired kidney function raises the risk of overshoot.

Principles that apply to all.

• Replace by the oral route when the gut works and the level is mildly low.
• Use the intravenous route for symptoms, arrhythmia, or inability to absorb.
• Use premixed, labelled products where available; never give concentrated potassium by bolus or push.
• Replace magnesium early, because low magnesium makes hypokalaemia and hypocalcaemia resistant to treatment.
• Recheck levels after each correction, then adjust.

Refeeding. In people who have eaten little for several days, starting feeding drives potassium, phosphate and magnesium into cells and can cause sudden low levels. Give thiamine before and with the first feeds, start feeding slowly and replace ions daily.

• First-line. Oral replacement for mild deficiency with a working gut; correction of the cause (stop or reduce a diuretic, treat diarrhoea or vomiting).
• Alternative. Potassium-sparing diuretics or ACE inhibitors to keep potassium up in people on chronic loop or thiazide diuretics.
• Specialist. Refeeding syndrome, renal tubular disorders, hypoparathyroidism, severe hypophosphataemia on intensive care.
• Emergency. Severe symptomatic hypokalaemia (arrhythmia), torsades de pointes (magnesium), symptomatic hypocalcaemia (tetany, seizure).

Selection. Treat the cause first. Choose the slowest safe route that works. Check kidney function before every prescription.

Contraindications. Potassium: hyperkalaemia, severe kidney failure without monitoring, untreated Addison disease. Magnesium: myasthenia gravis, heart block, severe kidney failure (reduce dose). Calcium: hypercalcaemia, digoxin toxicity (caution). Phosphate: hyperphosphataemia, hypocalcaemia that is not corrected, severe kidney failure.

Serious adverse effects.

• Potassium: cardiac arrhythmia, arrest, vein pain and phlebitis, gut ulceration from tablets.
• Magnesium: loss of reflexes, respiratory depression, hypotension, heart block.
• Calcium: arrhythmia, tissue necrosis if extravasated, hypercalcaemia.
• Phosphate: hypocalcaemia and tetany, soft-tissue calcification, diarrhoea.

Major interactions. ACE inhibitors, ARBs, spironolactone, trimethoprim and NSAIDs add to potassium; digoxin toxicity worsens with low potassium and with intravenous calcium; calcium binds tetracyclines, quinolones, levothyroxine and bisphosphonates; phosphate binds calcium and some antibiotics; magnesium adds to neuromuscular blockers.

Common prescribing errors.

• Giving potassium too fast or in a concentration too high for a peripheral vein.
• Replacing potassium without checking magnesium.
• Using concentrated ampoules without dilution.
• Giving calcium and phosphate in the same line.
• Not rechecking levels after replacement.

Special groups.

• Pregnancy: replace as needed; magnesium sulfate has specific obstetric uses.
• Breastfeeding: compatible at replacement doses.
• Children: weight-based doses; confirm with a paediatric formulary.
• Older adults: lower starting doses and more frequent checks.
• Kidney: reduce doses and recheck sooner; avoid magnesium and phosphate loads in severe failure.
• Liver: monitor, since cirrhosis changes fluid balance and ion levels.
• East Africa: premixed potassium and phosphate bags may not be available; where only concentrated ampoules exist, dilute under a written local procedure and label the bag; diarrhoeal disease, malnutrition and refeeding are common causes of deficit.

Monitoring. Serum potassium, magnesium, calcium, phosphate and creatinine at baseline and 4 to 6 hours after a correction; ECG during rapid replacement.

Referral and escalation. ECG changes, muscle weakness, seizure, abnormal rhythm, falling level despite replacement, or kidney failure.

Comparison with alternative classes. Replacement corrects the level directly and quickly, but needs careful rate control. Dietary change and treating the cause are safer for mild or chronic deficiency but act slowly.