Why Electrolyte Emergencies Are High-Yield
Hyponatraemia and hyperkalaemia are the two electrolyte disturbances most likely to appear in an OSCE, because both are common on the wards, both have classic and testable ECG or clinical findings, and both carry a real risk of iatrogenic harm if corrected incorrectly. Examiners are specifically checking whether you know the safe rate of correction for sodium and the immediate stabilising treatment for potassium, not just the underlying causes.
Hyponatraemia
Step 1: Assess Severity and Symptoms First
⚠️ Red Flag
Management is driven by symptoms and rate of onset, not just the sodium number. Severe symptomatic hyponatraemia (seizures, coma, GCS drop) requires urgent hypertonic saline regardless of the exact sodium level; mild chronic hyponatraemia in an asymptomatic patient requires a much more cautious, gradual approach.
Classify by severity:
- Mild: 130–135 mmol/L
- Moderate: 125–129 mmol/L
- Severe: <125 mmol/L, or any level with severe symptoms (seizures, reduced GCS, respiratory distress)
Step 2: Classify by Volume Status
🧠 Mnemonic
HEV for the three-way volume-status classification of hyponatraemia:
- Hypovolaemic (fluid loss exceeding sodium loss, e.g. diuretics, vomiting, diarrhoea, Addison's disease)
- Euvolaemic (SIADH, hypothyroidism, adrenal insufficiency, psychogenic polydipsia)
- Volume overloaded/hypervolaemic (heart failure, liver cirrhosis, nephrotic syndrome, renal failure)
Assess volume status clinically: skin turgor, mucous membranes, JVP, oedema, postural blood pressure, and review the drug chart (diuretics are a very common cause and easy to miss).
💎 Clinical Pearl
SIADH is diagnosed by finding euvolaemic hyponatraemia with inappropriately concentrated urine (urine osmolality >100 mosm/kg) and urine sodium >30 mmol/L, in the absence of adrenal, thyroid, or renal dysfunction, and typically with low plasma osmolality. Common causes: small cell lung cancer, pneumonia, meningitis, and drugs (SSRIs, carbamazepine).
Step 3: Treat According to Severity
| Presentation | Management |
|---|---|
| Severe/symptomatic (seizures, coma) | IV hypertonic saline (2.7% or 3%) in a monitored setting, aim to raise sodium by 4–6 mmol/L in the first few hours to reverse life-threatening symptoms, then slow down |
| Hypovolaemic | IV 0.9% saline to correct volume depletion |
| Euvolaemic (SIADH) | Fluid restriction (typically 500ml–1L/day); consider demeclocycline or vaptans if refractory (specialist input) |
| Hypervolaemic | Fluid restriction and treat the underlying cause (diuretics for heart failure, guided by specialists) |
⚠️ Red Flag
Never correct chronic hyponatraemia too fast. The maximum safe correction rate is generally no more than 8–10 mmol/L in 24 hours (some guidelines say even more cautious, 6 mmol/L, in high-risk patients: alcoholics, malnourished, liver disease, hypokalaemia). Overcorrection risks osmotic demyelination syndrome (central pontine myelinolysis), causing irreversible quadriparesis, dysarthria, and locked-in syndrome, typically appearing 2-6 days after overly rapid correction.
💎 Clinical Pearl
Memory aid: "Low and slow, unless they're about to blow." Chronic asymptomatic hyponatraemia is corrected low and slow; severe symptomatic hyponatraemia with imminent risk of brain herniation is the one exception where rapid initial correction is justified, followed immediately by slowing down once symptoms improve.
Hyperkalaemia
Recognising Severity
- Mild: 5.5–5.9 mmol/L
- Moderate: 6.0–6.4 mmol/L
- Severe: ≥6.5 mmol/L, or any level with ECG changes, this is a medical emergency
ECG Changes, In Order of Progression
🧠 Mnemonic
T-PQR-S for the progressive ECG changes of rising potassium:
- Tall tented T waves (earliest change)
- P wave flattening/widening, then disappearance
- QRS widening
- Risk of sine-wave pattern
- Sudden cardiac arrest (ventricular fibrillation or asystole) if untreated
⚠️ Red Flag
Any ECG changes in the presence of hyperkalaemia mean treatment must start immediately, do not wait for a repeat potassium level to confirm before giving calcium gluconate.
Emergency Management, In Order
🧠 Mnemonic
CBSD-T for hyperkalaemia emergency treatment, in the order given:
- Calcium gluconate 10ml of 10% IV, stabilises the cardiac membrane (does not lower potassium, buys time by protecting the heart)
- Beta-agonist (nebulised salbutamol), shifts potassium intracellularly
- Shift with insulin-dextrose, 10 units of short-acting insulin in 25g glucose (e.g. 50ml of 50% dextrose or equivalent), shifts potassium into cells over 15–60 minutes
- Diuresis or dialysis to actually remove potassium, if renal function allows, or urgent dialysis if renal failure/refractory
- Treat the underlying cause (review medications, e.g. ACE inhibitors, potassium-sparing diuretics; consider calcium resonium as a slower-acting adjunct, no longer routinely recommended acutely)
💎 Clinical Pearl
Calcium gluconate does not lower serum potassium. Students frequently misstate this. It stabilises the myocardial cell membrane against the arrhythmogenic effect of hyperkalaemia, buying time, while insulin-dextrose and salbutamol actually shift potassium into cells to lower the serum level. Only dialysis or diuresis actually removes potassium from the body.
Common Causes to Screen For
- Renal failure (acute or chronic), the most common cause on the wards
- Drugs: ACE inhibitors, ARBs, potassium-sparing diuretics (spironolactone, amiloride), NSAIDs, trimethoprim, suxamethonium
- Acidosis (potassium shifts extracellularly as hydrogen ions move intracellularly)
- Tissue breakdown: rhabdomyolysis, tumour lysis syndrome, haemolysis
- Adrenal insufficiency (loss of aldosterone effect)
- Pseudohyperkalaemia: haemolysed sample, prolonged tourniquet time, delayed processing, always consider repeating the sample if the result doesn't fit the clinical picture
Frequently Asked Questions
"Why do you give calcium gluconate before insulin-dextrose in severe hyperkalaemia?"
Calcium gluconate acts within minutes to stabilise the cardiac membrane and reduce the immediate risk of a fatal arrhythmia, but it does not change the serum potassium level. Insulin-dextrose takes 15–60 minutes to start shifting potassium intracellularly. Giving calcium first buys time for the slower-acting potassium-lowering treatments to work.
"What is the maximum safe rate of sodium correction in chronic hyponatraemia, and why?"
No more than 8–10 mmol/L in 24 hours (more cautious limits of around 6 mmol/L are used in high-risk patients such as those with alcohol excess, malnutrition, or liver disease). Correcting faster than this risks osmotic demyelination syndrome (central pontine myelinolysis), as brain cells that have adapted to a chronically low extracellular sodium cannot re-equilibrate quickly enough, causing osmotic injury to neurons, particularly in the pons.
"A patient's potassium comes back at 7.2 with no ECG changes reported, what do you do?"
Treat it as a medical emergency regardless of the ECG, get an ECG immediately if one hasn't been done, and start emergency management (calcium gluconate if any ECG changes are found, insulin-dextrose, nebulised salbutamol) without waiting, since a potassium this high carries a substantial risk of a sudden arrhythmia even if the current ECG looks reassuring.