Electrolyte Disorders: Hyponatraemia, Hypernatraemia, Hypokalaemia, Hyperkalaemia and Their Correction

Definition / Overview

• Electrolyte disorders are among the most common and clinically consequential abnormalities encountered in internal medicine.
• They represent not simply abnormal numbers but reflections of underlying pathophysiology, disordered volume regulation, hormonal dysregulation, drug toxicity, or end-organ failure.
• The FRACP candidate must be fluent in the bedside synthesis of history, examination, and investigation to reach a diagnosis, stratify urgency, and institute evidence-based treatment while avoiding iatrogenic harm (particularly from over-rapid correction).

Hyponatraemia

Definition and Classification

• Hyponatraemia is defined as a serum $\text{Na}^+$ below 135 mmol/L; clinically significant is typically <130 mmol/L.
• Classified by:
  • Onset: Acute (<48 hours) vs. chronic (≥48 hours or unknown), determines correction safety
  • Severity: Mild 130-135, Moderate 125-129, Profound <125 mmol/L
  • Volume status: Hypovolaemic, euvolaemic, or hypervolaemic

Pathophysiology

• Hyponatraemia almost universally reflects excess free water relative to sodium, not absolute sodium depletion.
• The key hormone is ADH (vasopressin), whose appropriate or inappropriate secretion drives water retention in the collecting duct.
• Exceptions include pseudohyponatraemia (hypertriglyceridaemia, hyperproteinaemia) and translocational hyponatraemia (hyperglycaemia, mannitol).

$$\text{Corrected Na}^+ = \text{Measured Na}^+ + 0.3 \times (\text{glucose} - 5.5)\,\text{mmol/L}$$

Aetiology by Volume Status

SIADH diagnostic criteria: Plasma $\text{Na}^+ < 135\,\text{mmol/L}$ with low plasma osmolality (<275 mOsmol/kg), urine osmolality >100 mOsmol/kg, urine $\text{Na}^+ > 20\,\text{mmol/L}$, clinically euvolaemic, absence of diuretics, hypothyroidism, or adrenal insufficiency.

Common SIADH causes: pulmonary disease (pneumonia, TB, malignancy), CNS disorders (stroke, meningitis, subdural haematoma), malignancy (small-cell lung cancer), drugs (opioids, SSRIs, carbamazepine, cyclophosphamide).

Clinical Features

• Mild-moderate: nausea, headache, cognitive slowing, gait disturbance
• Severe/acute: seizures, obtundation, herniation, respiratory arrest
• Chronic hyponatraemia often surprisingly asymptomatic, yet associated with falls, osteoporosis, and cognitive decline

Management

Assess urgency first, symptoms trump the number.

1. Severely symptomatic (seizures, coma): Hypertonic saline 3% NaCl, give 150 mL IV over 20 minutes, repeat if necessary, targeting symptom resolution and a rise in $\text{Na}^+$ of 5 mmol/L acutely. Seek ICU input.
2. Acute hyponatraemia (<48 h), even if asymptomatic: Correct more liberally; risk of cerebral oedema outweighs osmotic demyelination risk.
3. Chronic or unknown duration:
   • Target correction rate: ≤8-10 mmol/L per 24 hours, maximum 18 mmol/L per 48 hours
   • Exceeding this risks osmotic demyelination syndrome (ODS), previously called central pontine myelinolysis, a devastating, often irreversible demyelination
   • Higher-risk patients for ODS: $\text{Na}^+ < 105$, malnutrition, alcoholism, liver disease, hypokalaemia

Specific treatment by cause:

• Hypovolaemic: Cautious isotonic saline (0.9% NaCl), beware that as ADH suppresses after volume repletion, free water excretion accelerates and $\text{Na}^+$ may rise faster than anticipated (risk of ODS)
• SIADH: Fluid restriction (500-1000 mL/day) first-line; if refractory, consider demeclocycline, urea, or vaptans (tolvaptan), tolvaptan is effective but avoid in liver disease (risk of hepatotoxicity); avoid in hypovolaemia
• Hypervolaemic: Treat underlying cause; fluid restriction; loop diuretics in cardiac failure

Overcorrection protocol: If $\text{Na}^+$ rises too fast, administer $\text{DDAVP}$ (desmopressin) 2 mcg IV/SC + free water PO or 5% dextrose IV to halt further rise (the "clamp" technique).

Hypernatraemia

Definition and Pathophysiology

• Defined as serum $\text{Na}^+ > 145\,\text{mmol/L}$
• Always represents free water deficit relative to sodium, either water loss, inadequate intake, or (rarely) excessive sodium administration
• Intact thirst mechanism is normally highly protective; hypernatraemia implies impaired access to water or abnormal thirst (elderly, neurologically impaired, critically ill patients are most vulnerable)

Aetiology

• Differentiating DI: Urine osmolality inappropriately low (<300 mOsmol/kg) despite hypernatraemia.
• Urine osmolality >800 suggests extra-renal loss.
• Water deprivation test + DDAVP challenge distinguishes cranial from nephrogenic DI.

Clinical Features

• Thirst, irritability, confusion, weakness
• Severe: lethargy, seizures, coma; intracranial haemorrhage from cerebral dehydration (brain shrinkage tears bridging veins)
• Chronic hypernatraemia: brain accumulates idiogenic osmoles, correction must be gradual to avoid cerebral oedema

Management

1. Calculate free water deficit: $$\text{Free water deficit (L)} = 0.6 \times \text{body weight (kg)} \times \left(\frac{\text{Na}^+_{\text{measured}}}{140} - 1\right)$$

2. Acute hypernatraemia (<48 h): May correct more rapidly.

3. Chronic/unknown: Correct at ≤10-12 mmol/L per 24 hours to avoid cerebral oedema.
4. If $\text{Na}^+ \geq 170\,\text{mmol/L}$: Begin with 0.9% NaCl to avoid too rapid a drop; transition to 0.45% NaCl or 5% dextrose as level falls.
5. Oral/enteral water preferred if gut accessible.
6. Monitor $\text{Na}^+$ every 4-6 hours initially; adjust infusion rate based on trajectory.
7. Cranial DI: Desmopressin (intranasal, oral, or 2 mcg IM/SC), fluid replacement still essential alongside.
8. Nephrogenic DI: Treat underlying cause (lithium toxicity, hypercalcaemia); thiazide diuretics paradoxically reduce polyuria by inducing mild hypovolaemia, enhancing proximal tubular reabsorption; low-sodium, low-protein diet.

Hypokalaemia

Definition and Pathophysiology

• Serum $\text{K}^+ < 3.5\,\text{mmol/L}$; severe <2.5 mmol/L
• Most body potassium is intracellular (98%); serum levels reflect a small pool and can be misleading in acid-base disturbances
• Alkalosis and insulin drive $\text{K}^+$ intracellularly, masking total body depletion; acidosis shifts $\text{K}^+$ extracellularly

Aetiology

Hypomagnesaemia refractory to potassium replacement, check and replace $\text{Mg}^{2+}$ concurrently; $\text{Mg}^{2+}$ is required for renal $\text{K}^+$ conservation.

Clinical Features and ECG

• Muscle weakness, cramps, fatigue; severe: flaccid paralysis, respiratory failure
• Palpitations, ventricular ectopics, tachyarrhythmias
• ECG changes: flattened T waves, prominent U waves (particularly in lateral leads), prolonged QU interval, ST depression; severe hypokalaemia predisposes to ventricular tachycardia (including torsades de pointes) and potentiates digoxin toxicity

Management

• Oral replacement preferred when $\text{K}^+ > 2.5\,\text{mmol/L}$ and haemodynamically stable: potassium chloride (KCl) 40-80 mmol/day in divided doses
• IV replacement: KCl via central line at ≤20 mmol/hour (peripheral vein max 10 mmol/hour with dilution); maximum 40 mmol/hour via central line in life-threatening arrhythmia with continuous cardiac monitoring
• Treat hypomagnesaemia concurrently: $\text{MgSO}_4$ 10 mmol IV over 30-60 minutes
• Address underlying cause (stop offending diuretic, treat hyperaldosteronism)
• Cardiac patients and digoxin users: Maintain $\text{K}^+ \geq 4.0\,\text{mmol/L}$

Hyperkalaemia

Definition and Risk Stratification

• Serum $\text{K}^+ > 5.5\,\text{mmol/L}$; emergency level ≥6.5 mmol/L or any level with ECG changes
• First exclude artefact: haemolysis (red cells release $\text{K}^+$), thrombocytosis, prolonged sample transport, if clinical picture doesn't fit, repeat promptly

Aetiology

Clinical Features and ECG

Symptoms are often absent until severe; the ECG is the essential monitoring tool.

Non-cardiac: muscle weakness, paraesthesiae, ascending paralysis, nausea

Stepwise Acute Management

1. Attach cardiac monitor; obtain 12-lead ECG immediately
2. IV access and bloods: Repeat $\text{K}^+$, renal function, bicarbonate, glucose, calcium

3. Membrane stabilisation (if ECG changes or $\text{K}^+ > 6.5\,\text{mmol/L}$):

   • $\text{CaCl}_2$ 10% solution 10 mL IV over 5-10 minutes (or calcium gluconate 10% 30 mL via peripheral vein)
   • Onset within 1-3 minutes; duration 30-60 minutes; does not lower $\text{K}^+$
   • Repeat if ECG does not normalise in 5 minutes

4. Transcellular shift (buy time while elimination is arranged):

   • Insulin-dextrose: actrapid 10 units IV + 50 mL of 50% glucose (or 125 mL of 20% glucose), lowers $\text{K}^+$ by 0.5-1.5 mmol/L within 15-30 minutes; monitor BSL
   • Nebulised salbutamol 10-20 mg, additive effect, onset 30 minutes; note: unreliable in cardiac patients and not effective in all individuals
   • Sodium bicarbonate 8.4% 50 mmol IV, primarily useful in concurrent severe metabolic acidosis; modest $\text{K}^+$-lowering effect in isolation

5. Elimination (remove $\text{K}^+$ from the body):

   • Furosemide 40-80 mg IV if urine output adequate and volume status allows
   • Resonium (sodium polystyrene sulfonate) or patiromer orally/PR, onset hours; limited evidence for acute use; resonium can cause GI necrosis, use with caution
   • Dialysis: most effective; indicated for anuric AKI, refractory hyperkalaemia, or $\text{K}^+ > 7.0\,\text{mmol/L}$ with haemodynamic instability

6. Address precipitating cause: Stop causative drugs (ACEi, ARB, spironolactone, NSAIDs), treat acidosis, manage AKI

Complications & Special Considerations

Osmotic Demyelination Syndrome

• Risk with too-rapid correction of chronic hyponatraemia
• Particularly in: serum $\text{Na}^+ < 105\,\text{mmol/L}$, alcoholism, malnutrition, liver disease, concurrent hypokalaemia
• Presents subacutely 2-6 days after correction: dysarthria, dysphagia, pseudobulbar palsy, quadriparesis, "locked-in" syndrome
• MRI T2/FLAIR: pontine and extrapontine signal
• No proven treatment; prevention is paramount

Hyperkalaemia in CKD and RAAS Therapy

• Balancing act: ACE inhibitors/ARBs are renoprotective and cardioprotective (heart failure, diabetic nephropathy) but drive hyperkalaemia
• New potassium binders (patiromer, sodium zirconium cyclosilicate) allow continuation of RAAS therapy in CKD patients who would otherwise have needed dose reduction
• Discuss with nephrology before withdrawing RAAS therapy solely for hyperkalaemia in high-benefit patients

Perioperative and ICU Contexts

• Correct $\text{K}^+ < 3.0\,\text{mmol/L}$ before elective surgery (arrhythmia risk)
• Suxamethonium (succinylcholine) is contraindicated when $\text{K}^+$ is already elevated (can acutely raise $\text{K}^+$ by 0.5-1 mmol/L; catastrophic in burns, rhabdomyolysis, denervation injury)
• In DKA, total body $\text{K}^+$ is depleted despite apparent normo/hyperkalaemia; as insulin is given, $\text{K}^+$ falls precipitously, commence $\text{KCl}$ replacement early once $\text{K}^+ < 5.5\,\text{mmol/L}$

Long-Case Integration and Exam Approach

Viva Framing for Electrolyte Cases

• Always interpret an electrolyte result in clinical context: what is the volume status? what is the urine telling you?
• Avoid reflexive treatment, determine acuity and chronicity before acting
• Pair every electrolyte disorder with a medication reconciliation: diuretics, ACE inhibitors, ARBs, NSAIDs, laxatives, supplements, and corticosteroids are implicated across the spectrum

Key Formulae Summary

Safety Limits for Correction