Potassium and sodium emergencies

Hyperkalaemia: Emergency Management

Serum potassium $> 5.5\text{ mmol/L}$ constitutes hyperkalaemia, with levels $> 6.5\text{ mmol/L}$ or any potassium elevation associated with ECG changes constituting a medical emergency.

ECG Evolution in Hyperkalaemia

1. Tall, peaked, symmetrical T waves with a narrow base (earliest finding)
2. Prolongation of the PR interval and flattening or loss of P waves
3. Widening of the QRS complex
4. Merging of the wide QRS with the T wave forming a sine wave appearance
5. Ventricular fibrillation, idioventricular rhythm, or asystole

Stepwise Management Algorithm

1. Step 1: Cardiac Membrane Stabilization (Immediate):
   • Membrane protection: Give IV calcium for hyperkalaemic ECG toxicity under the local monitored protocol and repeat if needed. Calcium gluconate and calcium chloride have different elemental calcium concentrations; equal 10-mL volumes are not equivalent. Calcium stabilises the myocardium but does not remove potassium.
   • Mechanism: Antagonizes potassium-induced membrane excitability, normalizing threshold potential without lowering serum potassium levels.
   • Onset & Duration: Onset in $1 - 3\text{ minutes}$; duration of effect $30 - 60\text{ minutes}$. Repeat dose after 5-10 minutes if ECG changes persist.
2. Step 2: Intracellular Potassium Shifting (Within 15-30 minutes):
   • Intravenous Insulin with Glucose: Short-acting insulin (Actrapid $10\text{ units}$) added to $50\text{ mL}$ of $50\%$ dextrose (or $100\text{ mL}$ of $20\%$ dextrose) infused over 15 to 30 minutes. Stimulates the $\text{Na}^+/\text{K}^+$-ATPase pump, lowering serum potassium by $0.5 - 1.2\text{ mmol/L}$ within 30-60 minutes.
   • Nebulised Salbutamol: $10 - 20\text{ mg}$ via nebuliser (high dose, four times the asthma dose). $\beta_2$-adrenoceptor stimulation activates $\text{Na}^+/\text{K}^+$-ATPase.
   • Sodium Bicarbonate $8.4\%$: $50 - 100\text{ mL}$ IV over 10-20 minutes, indicated only if concurrent severe metabolic acidosis ($pH < 7.15$) is present.
3. Step 3: Total-Body Potassium Elimination:
   • Loop Diuretics: Intravenous frusemide ($40 - 80\text{ mg}$) in volume-replete patients with functioning kidneys.
   • Potassium Binders: Sodium zirconium cyclosilicate (SXC, Lokelma) or patiromer exchange potassium in the gastrointestinal tract.
4. Step 4: Emergency Haemodialysis (The AEIOU Criteria):
   • Acidosis: Severe refractory metabolic acidosis ($pH < 7.15$).
   • Electrolytes: Persistent, refractory hyperkalaemia ($> 6.5\text{ mmol/L}$) or recurrent malignant arrhythmias.
   • Ingestions: Toxic dialysable drugs (lithium, toxic alcohols, salicylates, metformin).
   • Overload: Refractory pulmonary oedema unresponsive to high-dose loop diuretics.
   • Uraemia: Uraemic pericarditis, uraemic encephalopathy, asterixis, or uraemic bleeding diathesis.

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Hyponatraemia: Diagnostic Classification & Correction Limits

Hyponatraemia (serum sodium $< 135\text{ mmol/L}$) is the most common electrolyte disorder in hospitalized patients.

Diagnostic Algorithm for Hypotonic Hyponatraemia

Syndrome of Inappropriate ADH Secretion (SIADH)

• Essential Diagnostic Criteria:
  1. Hypotonic hyponatraemia (plasma osmolality $< 275\text{ mOsm/kg}$)
  2. Inappropriately concentrated urine (urine osmolality $> 100\text{ mOsm/kg}$, typically $> 300\text{ mOsm/kg}$)
  3. Elevated urine sodium (urine $\text{Na} > 30\text{ mmol/L}$ despite normal dietary intake)
  4. Euvolaemic state on physical examination (no peripheral oedema, normal jugular venous pressure, normal skin turgor)
  5. Normal adrenal, thyroid, and renal function, without concurrent diuretic therapy
• Causes: Malignancy (small cell lung carcinoma in $> 70\%$ of paraneoplastic cases), central nervous system disorders (stroke, trauma, meningitis), pulmonary infections (pneumonia, tuberculosis), and drugs (SSRIs, carbamazepine, antipsychotics, PPIs, cyclophosphamide).
• SIADH: Confirm hypotonic hyponatraemia and exclude adrenal deficiency, thyroid disease and relevant drugs. Fluid restriction is usual initial treatment when appropriate, tailored to intake/output and feasibility; oral urea or other specialist treatment may be needed. Tolvaptan is not a generic routine second-line choice and can overcorrect sodium.

Acute Hyponatraemia with Severe Neurological Symptoms

• Patients presenting with severe neurovascular compromise (generalized tonic-clonic seizures, coma, respiratory depression, or signs of brainstem herniation) require emergent hypertonic saline.
• Treatment: Infuse hypertonic $3\%$ sodium chloride as a $100 - 150\text{ mL}$ IV bolus over 10 to 20 minutes. Repeat up to twice if severe symptoms persist, aiming for an immediate safe rise of $4 - 6\text{ mmol/L}$ to abort cerebral oedema.

The Golden Rule of Chronic Hyponatraemia: Safe Correction Limits

• In chronic hyponatraemia ($> 48\text{ hours}$), brain cells adapt to hypotonicity by extruding intracellular osmolytes (myo-inositol, glutamate) to prevent cerebral swelling.
• Rapid Correction Danger: Overly rapid sodium correction draws water out of brain cells, causing dehydration, blood-brain barrier disruption, and oligodendrocyte apoptosis leading to Osmotic Demyelination Syndrome (ODS) (formerly central pontine myelinolysis). Manifestations appear 2-6 days later: dysarthria, dysphagia, flaccid quadriparesis transitioning to spasticity, 'locked-in' syndrome, and permanent vegetative state.
• Maximum Safe Correction Limit: $\le 8\text{ mmol/L}$ in any 24-hour period (and $\le 4-6\text{ mmol/L}$ in patients with high risk: chronic alcoholism, malnutrition, advanced cirrhosis, hypokalaemia).
• Emergency Re-lowering: If accidental overcorrection occurs, immediately cease hypertonic/isotonic fluids, administer intravenous $5\%$ dextrose, and give desmopressin (DDAVP) to halt urinary free water loss.

Monitoring potassium and sodium treatment

After insulin/dextrose for hyperkalaemia, monitor glucose for several hours, particularly in renal failure; delayed hypoglycaemia can occur. Repeat potassium and ECG because shifting treatment is temporary and rebound is possible. Stop potassium sources and arrange definitive removal, including dialysis when indicated.

For severe symptomatic hyponatraemia, use monitored hypertonic saline under the emergency pathway, often initially targeting a 4–6 mmol/L rise sufficient to control symptoms. High-risk patients should not exceed 8 mmol/L in any 24 hours. Check sodium frequently and obtain urgent advice for overcorrection, potentially requiring desmopressin and controlled free-water replacement. A ceiling is not the intended daily target.

Primary references (checked 7 October 2026): KDIGO CKD guidance.