Electrolyte Disorders (Potassium, Sodium, Magnesium)

Electrolyte abnormalities are usually found incidentally on routine bloods rather than through symptoms, but severe derangement causes cardiac arrhythmias and is a medical emergency. The decision that matters in general practice is which abnormality can be managed in the community and which needs same-day hospital referral.

Hyperkalaemia

Causes: reduced excretion (ACE inhibitors, ARBs, potassium-sparing diuretics, NSAIDs, chronic kidney disease, adrenal insufficiency), increased intake (dietary, potassium supplements, salt substitutes), and shift out of cells (acidosis, tissue breakdown, insulin deficiency). Rule out pseudohyperkalaemia first — haemolysis of the sample, a prolonged tourniquet, or fist-clenching during venepuncture are common causes; repeat the test if there’s no other risk factor or ECG change.

Hyperkalaemia is usually asymptomatic until arrhythmias develop, so always get an ECG once potassium is confirmed elevated. ECG changes progress from peaked T waves and a shortened QT, to a widened QRS and loss of the P wave, to a sine-wave pattern and ventricular fibrillation or asystole.

Management by severity:

• Potassium <6 mmol/L with no ECG changes — reduce intake, stop potassium-elevating drugs, consider a loop diuretic if not volume-depleted; recheck to confirm resolution.
• Potassium 6–6.5 mmol/L — the above if no ECG changes and renal function is intact; otherwise treat as severe.
• Potassium >6.5 mmol/L, or any ECG change — needs urgent treatment and same-day hospital transfer: IV calcium to stabilise the myocardium (effect within minutes, lasts 20–30 minutes, may need repeating), IV insulin with glucose to shift potassium intracellularly (peaks at 1 hour, lasts several hours), and a nebulised high-dose beta-2 agonist as an adjunct. Potassium-binding resins remove potassium from the gut but act slowly. Arrange dialysis early for patients with significant chronic kidney disease or acute kidney injury.

Hypokalaemia

Causes: GI losses (vomiting, diarrhoea, laxative misuse), renal losses (diuretics, mineralocorticoid excess, renal tubular disorders), and intracellular shift (insulin, beta-agonists, alkalosis). Hypomagnesaemia commonly coexists and drives ongoing renal potassium wasting — check magnesium alongside potassium, since hypokalaemia won’t correct until magnesium is replaced.

Severity: mild (3.0–3.4 mmol/L) is usually asymptomatic; moderate (2.5–3.0 mmol/L) causes muscle weakness; severe (<2.5 mmol/L) causes ECG changes (ST sagging, T-wave flattening, prominent U waves) and risks atrial/ventricular arrhythmias.

Management: oral potassium chloride replacement (typically 20–80 mmol/day) is appropriate for mild-to-moderate hypokalaemia without ECG changes or severe symptoms — this can be managed in general practice with follow-up bloods. Severe hypokalaemia, ECG changes, or an arrhythmia need same-day hospital referral for IV replacement under cardiac monitoring — routine IV potassium runs no faster than 10 mmol/hour, and only in the setting of arrhythmia, under continuous monitoring, can it be given faster (up to 40 mmol/hour via a central line).

Hyponatraemia

Hyponatraemia (serum sodium <135 mmol/L) is the most common electrolyte abnormality and is usually a marker of underlying disease rather than a primary problem. Severe hyponatraemia (<120 mmol/L) is a medical emergency with substantially increased morbidity and mortality.

Classify by volume status to find the cause:

• Euvolaemic — the most common pattern: SIADH (drugs, malignancy, CNS or pulmonary disease, postoperative pain), hypothyroidism, hypocortisolaemia, primary polydipsia.
• Hypovolaemic — GI losses, salt-losing nephropathy, thiazide diuretics, cerebral salt wasting.
• Hypervolaemic — cardiac failure, cirrhosis, renal failure, nephrotic syndrome; usually obvious from history and examination.

GP management: mild, chronic, asymptomatic hyponatraemia (commonly euvolaemic) can often be managed in the community by treating the underlying cause and, in SIADH, fluid restriction. Any symptomatic or severe hyponatraemia (confusion, seizures, reduced consciousness, or sodium approaching 120 mmol/L) needs same-day hospital referral — treatment (usually hypertonic saline, with 24-hour pathology and often intensive care) is not something to start in general practice.

Never correct hyponatraemia too fast. Over-rapid correction, or overshooting above the normal range, causes osmotic (cerebral) demyelination — irreversible and often fatal, and it may not appear for several days after treatment. The maximum safe correction rate is 10 mmol/L in 24 hours (18 mmol/L in 48 hours); this is why severe hyponatraemia is managed in hospital under close monitoring rather than corrected empirically.

Hypomagnesaemia

Magnesium is easy to overlook, but deficiency drives refractory hypokalaemia and hypocalcaemia, and both hypo- and hypermagnesaemia can precipitate arrhythmias. Causes of hypomagnesaemia include malabsorption (IBD, chronic pancreatitis, alcoholism), GI losses (vomiting, nasogastric suction), and renal losses (loop/thiazide diuretics, aminoglycosides, amphotericin B, hypercalcaemia).

Management: asymptomatic or mild deficiency responds to oral magnesium supplements (e.g. magnesium aspartate 2–4 tablets/day in divided doses — higher doses cause diarrhoea, which limits the dose). Symptomatic hypomagnesaemia, or a level below 0.4 mmol/L, needs IV magnesium — oral correction takes roughly six weeks against about a week for IV. Correct hypokalaemia and hypomagnesaemia together, since potassium replacement won’t hold while magnesium remains low.

Hypermagnesaemia is almost always due to reduced renal excretion (renal failure, often compounded by magnesium-containing antacids or laxatives) — avoid magnesium-containing products in patients with renal impairment.

Referral

• Potassium >6.5 mmol/L, or any ECG change from hyper- or hypokalaemia — same-day hospital transfer.
• Symptomatic hyponatraemia (confusion, seizures, reduced GCS) or sodium approaching/below 120 mmol/L — same-day hospital referral; do not attempt correction in the community.
• Severe hypomagnesaemia (<0.4 mmol/L) or a symptomatic patient — needs IV replacement, arrange same-day assessment.
• Any electrolyte abnormality where the underlying cause itself needs urgent hospital work-up (e.g. new adrenal insufficiency, significant acute kidney injury).

Follow-up and safety-netting

Recheck levels after starting or stopping a causative drug, and after any oral replacement, to confirm correction and detect overshoot.

Warn patients on ACE inhibitors/ARBs, potassium-sparing diuretics or potassium supplements about the symptoms of hyperkalaemia — weakness, palpitations — and to avoid salt substitutes, which are usually potassium chloride.