Description
- Acute electrolyte derangements requiring urgent recognition and correction - hyponatraemia, hyperkalaemia, hypercalcaemia are the highest-yield emergencies; hypocalcaemia and hypomagnesaemia matter chiefly for their cardiac/neuromuscular effects and interactions with the others
- The correction rate itself can be the dangerous part - overly rapid correction of chronic hyponatraemia, or under-treatment of severe hyperkalaemia, each kill by a different mechanism
Epidemiology
- Hyponatraemia - commonest electrolyte disorder in hospitalised patients
- Hyperkalaemia - common with CKD, RAAS-blocker use, and in acute kidney injury
- Hypercalcaemia - malignancy and primary hyperparathyroidism together account for >90% of cases (malignancy dominates in inpatients, primary hyperparathyroidism in outpatients)
Aetiopathogenesis
Hyponatraemia - classify by volume status
- Hypovolaemic - GI/renal/skin losses with inadequate replacement
- Euvolaemic - SIADH (malignancy, CNS/pulmonary disease, drugs), hypothyroidism, adrenal insufficiency, psychogenic polydipsia
- Hypervolaemic - heart failure, cirrhosis, nephrotic syndrome (effective circulating volume depletion despite total body Na+ excess)
Hyperkalaemia
- Reduced excretion - AKI/CKD, RAAS blockers (ACEi/ARB/MRA), potassium-sparing diuretics, adrenal insufficiency
- Transcellular shift - acidosis, insulin deficiency, tissue breakdown (rhabdomyolysis, tumour lysis, haemolysis), beta-blockade
- Pseudohyperkalaemia - haemolysed sample, prolonged tourniquet time, marked thrombocytosis/leukocytosis - always consider before treating an unexpected result
Hypercalcaemia
- Malignancy - PTHrP-mediated (squamous cell carcinomas), osteolytic bone metastases, or rarely ectopic 1,25-OH vitamin D (lymphoma)
- Primary hyperparathyroidism - autonomous PTH secretion (adenoma most commonly)
- Others: vitamin D toxicity, granulomatous disease (sarcoidosis), thiazides, immobilisation, milk-alkali syndrome
Diagnosis
Hyponatraemia
- Assess volume status clinically first, then serum/urine osmolality and urine sodium to classify mechanism
- Severity by symptoms (confusion, seizure, coma) matters more for urgency than the absolute number alone, though very low levels (<120mmol/L) or rapid onset raise risk
Hyperkalaemia
- ECG is the priority investigation - peaked T waves -> widened QRS -> sine wave pattern -> VF/asystole; ECG changes (or K+ >6.5mmol/L) define an emergency requiring immediate treatment, not the number alone
- Repeat on a clean non-haemolysed sample if result unexpected/asymptomatic
Hypercalcaemia
- PTH level is the key discriminator: elevated/inappropriately normal PTH -> primary hyperparathyroidism; suppressed PTH -> malignancy or other non-PTH-mediated cause
- Corrected calcium (albumin-adjusted) or ionised calcium; ECG (short QT interval)
Management
A. Hyponatraemia
- Severe symptomatic (seizure, coma) - hypertonic (3%) saline in small boluses to acutely raise sodium enough to relieve cerebral oedema symptoms, then slow
- Correction rate limit is the critical safety point: no more than ~8mmol/L rise per 24 hours (more conservative, ~4-6mmol/L/24h, in high-risk patients - alcoholics, malnourished, hypokalaemic, liver disease) - exceeding this risks osmotic demyelination syndrome
- Treat by volume status and cause: fluid restriction (SIADH), isotonic saline (hypovolaemic), diuretic + fluid restriction (hypervolaemic)
- Overcorrection occurring rapidly (e.g. from a large spontaneous water diuresis) can itself need active re-lowering with desmopressin + free water - a key modern safety practice
B. Hyperkalaemia
- ECG changes or K+ >6.5mmol/L - treat immediately, do not wait for a repeat level
1. IV calcium gluconate - stabilises the cardiac membrane, does not lower potassium, works within minutes
2. Insulin + glucose (IV) - shifts potassium intracellularly, onset ~15-30 min
3. Salbutamol (nebulised, high dose) - additional shift, adjunct not substitute
4. Potassium binders (sodium zirconium cyclosilicate, patiromer) or resonium - remove potassium from the body, slower onset, for ongoing/sustained lowering
5. Dialysis - definitive for severe/refractory hyperkalaemia, especially with significant renal failure
- Address the precipitant - stop/hold RAAS blockers acutely, treat acidosis, treat rhabdomyolysis/tumour lysis if present
C. Hypercalcaemia
- IV isotonic saline rehydration first - most patients are volume-depleted (calcium impairs renal concentrating ability)
- IV bisphosphonate (zoledronic acid) - mainstay for malignancy-associated hypercalcaemia, takes 2-4 days for full effect
- Calcitonin - rapid onset, short-lived effect, useful as a bridge while bisphosphonate takes effect
- Denosumab - option in bisphosphonate-refractory cases or renal impairment (bisphosphonates renally cleared)
- Loop diuretics - only after adequate rehydration, not as an isolated first step, and not routinely required
- Primary hyperparathyroidism - definitive treatment is parathyroidectomy once criteria met
Associations
- Hyponatraemia - SIADH-associated malignancy/CNS/pulmonary disease, heart failure, cirrhosis, nephrotic syndrome, thiazide use
- Hyperkalaemia - CKD, RAAS blockade, adrenal insufficiency, rhabdomyolysis, tumour lysis syndrome
- Hypercalcaemia - malignancy (squamous cell carcinomas, myeloma, breast), primary hyperparathyroidism, sarcoidosis, thiazides, immobilisation
Natural history & complications
- Hyponatraemia - untreated severe/acute cases risk cerebral oedema/herniation; overly rapid correction of chronic hyponatraemia risks osmotic demyelination syndrome (often delayed 2-6 days, can be irreversible)
- Hyperkalaemia - untreated progression to fatal arrhythmia (VF, asystole) can occur rapidly, especially with a widening QRS
- Hypercalcaemia - untreated severe cases cause nephrogenic diabetes insipidus, nephrocalcinosis/AKI, arrhythmia, and coma ("stones, bones, groans, psychiatric overtones")
- Recurrent electrolyte crises usually indicate an unaddressed underlying driver (malignancy progression, medication non-adjustment, undiagnosed endocrinopathy) - correcting the number without addressing the cause invites recurrence
7 of 7 sections written · drafted 2026-09-14