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Hyponatraemia

Background Information

Definition

Hyponatraemia is defined as serum sodium <135 mmol/L

The general cut-off of severe hyponatraemia is <120 mmol/L

Clinical Features

Clinical features of hyponatraemia are highly non-specific.
Clinical features in moderately severe hyponatraemia:

  • Nausea (without vomiting)
  • Confusion
  • Headache

Clinical features in severe hyponatraemia (from cerebral oedema):

  • Vomiting
  • Abnormal and deep somnolence
  • Cardiorespiratory depress
  • Seizures
  • Coma
  • Hyporeflexia

Also, varying fluid status and features of the underlying cause.

Sodium disturbances (hypernatraemia or hyponatraemia) do NOT typically cause ECG changes or arrhythmias.

Unlike abnormalities in potassium, calcium, or magnesium, which directly affect cardiac electrophysiology.

Complications

Key complication of acute hyponatraemia: cerebral oedema

Complications of chronic hyponatraemia:

  • Cognitive deficits
  • Gait disturbances
  • Falls
  • Fragility fractures

Diagnosis

Diagnostic Approach

Key tests to order

  • Non-specific tests (to categorise the hyponatraemia)
    • Paired serum and urine osmolality
    • Paired serum and urine electrolytes
    • Serum glucose level
    • Fluid status assessment

 

  • Specific tests
    • Renal function (urea, creatinine, eGFR)
    • TFT (to exclude hypothyroidism)
    • Serum cortisol (to exclude adrenal insufficiency)

Identifying the Underlying Cause of Hyponatraemia

The causes of hyponatraemia are first classified based on serum osmolality.

Hypotonic Hyponatraemia (True Hyponatraemia)

Real, physiological reduction in plasma sodium concentration, leading to a decrease in serum osmolality

Causes are sub-classified by fluid status and renal sodium:

Renal causes (urine sodium >20 mmol/L) Extra-renal cause (urine sodium  ≤20 mmol/L)
Hypovolaemic
  • Diuretics (thiazide diuretics ++)
  • Polyuric renal failure (mainly recovery phase of ATN and post-obstructive diuresis)
  • Cerebral salt wasting syndrome
  • GI losses (vomiting, diarrhoea, high stoma output, fistula)
  • Burns
  • Excessive sweating
  • Bleeding
  • 3rd space fluid loss (e.g. pancreatitis, ascites, peritonitis)
Euvolaemic
  • SIADH – most common (see this article for more details)
  • Adrenal insufficiency
  • Hypothyroidism
  • Reduced oral salt intake (e.g. “tea and toast” diet)
  • Primary polydipsia
Hypervolaemic
  • Anuric / oliguric renal failure (typical CKD and AKI causes)
  • Congestive heart failure
  • Liver cirrhosis
  • Nephrotic syndrome

Fluid status:

  • Hypovolaemic: ↓ skin turgor, dry mucous membrane, tachycardia, hypotension
  • Hypervolaemic: peripheral oedema, ↑ JVP, pulmonary oedema (bi-basal crackles)

Isotonic Hyponatraemia

Causes:

  • Pseudohyponatremia (laboratory artefact, caused by hyperlipidaemia, multiple myeloma)
  • TURB syndrome

Hypertonic Hyponatremia

Causes:

  • Hyperglycaemia
  • Severe uraemia
  • Mannitol use

Management

Severe, Symptomatic Hyponatraemia (<120 mmol/L)

Treat immediately with hypertonic saline (options include 3%, 2.7%, 1.8% saline)

  • Patient should be in HDU / ICU, under the guidance of a senior
  • The aim is to improve symptoms, NOT correct sodium back to normal

Other Patients

If hypertonic saline is not necessary (see above), hyponatraemia is treated depending on fluid status and likely underlying cause

Fluid status Management
Hypovolaemic Treat with 0.9% saline
Euvolaemic Depends on the underlying cause:
  • SIADH (most common) → fluid restriction
  • Hypothyroidism → treat accordingly with levothyroxine
  • Adrenaline insufficiency → treat accordingly with steroid replacement
Hypervolaemic Fluid restriction +/- diuretics needed

Exact management depends on the underlying cause (usually due to AKI / heart failure / cirrhosis / nephrotic syndrome)

It is important NOT to correct hyponatraemia too quickly, due to the risk of osmotic demyelination syndrome (rapid increase of serum osmolality will cause water shifting out of the brain cells rapidly, leading to dehydration and injury of oligodendrocytes)

To prevent osmotic demyelination syndrome from occurring:

  • Maximum correction rate is 10 mmol/L in the first 24 hours
  • Then, 8 mmol/L in the subsequent 24 hours

On the other hand, if hypernatraemia is corrected too rapidly, there is a risk of developing cerebral oedema (rapid reduction of serum osmolality will cause water shifting into brain cells rapidly).

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