IM23.4-7 | Sodium and Potassium Disorders — Summary & Reflection

KEY TAKEAWAYS

Hyponatraemia (Na <135 mmol/L) — a disorder of water excess relative to sodium. Diagnostic sequence: (1) serum osmolality → exclude pseudohyponatraemia and hypertonic causes; (2) volume status; (3) urine Na and urine osmolality. SIADH: euvolaemic + hypotonic + inappropriately concentrated urine (>100 mOsm/kg) + urine Na >40 + normal thyroid/adrenals. Safe correction limit: ≤10–12 mmol/L/24 hours. Overcorrection risk: osmotic demyelination syndrome. Acute symptomatic (seizures/coma): 3% hypertonic saline 100 mL bolus. Chronic euvolaemic: fluid restriction ± tolvaptan.

Hypernatraemia (Na >145 mmol/L) — free water deficit. Causes: insensible losses, diabetes insipidus (CDI: responds to desmopressin; NDI: does not), osmotic diuresis. Treatment: replace free water deficit with hypotonic fluids, max correction 0.5–1 mmol/L/hour.

Hypokalaemia (K <3.5 mmol/L) — renal losses (urine K >20 mmol/L: diuretics, hyperaldosteronism, hypomagnesaemia) vs extrarenal (urine K <20 mmol/L: GI losses). ECG: U waves, T flattening, QT prolongation. Treat cause + replace K (oral preferred; IV max 20 mmol/hr peripheral). Always check and correct Mg²⁺.

Hyperkalaemia (K >5.0 mmol/L) — causes: CKD, RAAS drugs, acidosis, rhabdomyolysis. ECG sequence: peaked T → PR prolongation → P loss → wide QRS → sine wave. Emergency treatment in sequence: (1) IV calcium gluconate (membrane stabilisation, acts 1–3 min); (2) insulin + dextrose ± salbutamol (transcellular shift, 15–30 min); (3) frusemide, resins, or dialysis (removal, hours). Insulin-dextrose without calcium first = dangerous if ECG abnormal.

REFLECT

Return to Patient B from the opening scenario — the 55-year-old man with CKD and a potassium of 6.8 mmol/L on ECG showing peaked T waves and a prolonged PR interval. The registrar's plan was to 'monitor and repeat K tomorrow morning.' Reflect on the physiological trajectory: from peaked T waves at 6.8 mmol/L, this patient is one step away from P wave loss and then wide QRS — potentially fatal ventricular fibrillation. Without membrane stabilisation with IV calcium gluconate immediately, the eight-hour wait for a repeat measurement could be the interval in which cardiac arrest occurs. Now consider Patient A — the woman with pneumonia whose sodium was overcorrected by 16 mmol/L overnight. She has not yet developed symptoms of osmotic demyelination, but the risk window is now. What would you do: continue monitoring, or actively intervene to relower the sodium? Thinking through these two cases in parallel illustrates the core principle this module seeks to instil: electrolyte disorders require not just knowledge of normal ranges, but the clinical judgment to recognise emergency from stable, and the discipline to act in the correct physiological sequence.