Hyponatraemia

Serum sodium concentration is maintained by a homeostatic mechanism that involves thirst, anti-diuretic hormone (ADH) secretion and the renal handling of sodium. This is defined as a serum sodium <135mmol/l.¹ A level <120mmol/l is considered severe.²

Falsely low sodium values results can occur with very high circulating levels of lipids or proteins in which the concentration of sodium in the water phase is normal (plasma osmolality normal). This can also occur in severe hyperglycaemia as the high levels of glucose draw intracellular water into the extracellular space.

Hyponatraemia is the commonest electrolyte abnormality encountered in clinical practice. An accurate incidence of mild Hyponatraemia managed in the community is impossible as it is rarely reported. Most figures therefore concern hospitalised patients.³ A study in a surgical ward showed that approximately 4.4% of postoperative patients developed Hyponatraemia within 1 week of surgery. It has also been observed in approximately 30% of patients treated in an intensive care unit.¹

These depend upon severity and are dictated not only by the absolute serum sodium level but also by the rate of fall. Thus chronic mild Hyponatraemia may be asymptomatic whilst a sudden fall to only 125mmol/l from normal values can result in convulsions (usually from inappropriate intravenous fluids).

Symptoms

• Mild - anorexia, headache, nausea, vomiting, lethargy
• Moderate - personality change, muscle cramps and weakness, confusion, ataxia
• Severe - drowsiness

Signs

These are again highly variable and depend on the level and rate of fall of the serum sodium. They may include:

• Neurological signs
  • Decreased level of consciousness
  • Cognitive impairment (e.g. short-term memory loss, disorientation, confusion depression)
  • Focal or generalised seizures
  • Brain stem herniation - seen in severe acute Hyponatraemia; signs include coma; fixed, unilateral, dilated pupil, decorticate or decerebrate posturing, respiratory arrest
• Signs of hypovolaemia - dry mucous membranes, tachycardia, diminished skin turgor
• Signs of hypervolaemia - pulmonary rales, S3 gallop (third heart sound), jugular venous distention, peripheral oedema, ascites

• Plasma hypo-osmolality proportional to Hyponatraemia.
• Urine osmolality >plasma osmolality
• Persistent renal sodium excretion of around 50-70mmol/l
• Normal renal, thyroid and adrenal function

The causes of Hyponatraemia can be divided into three groups:

• Hypovolaemic
• Normovolaemic
• Hypervolaemic

• Adrenal insufficiency and adrenal crisis
• Congestive heart failure and pulmonary oedema
• Gastroenteritis
• Hypothyroidism and myxoedema
• Coma
• Renal failure - acute, chronic and dialysis complications
• Syndrome of Inappropriate Anti-diuretic Hormone Secretion
• Cirrhosis
• Nephrotic syndrome
• Psychogenic polydipsia
• PseudoHyponatraemia (falsely low sodium reading due to presence of excessive high weight molecules in the serum, such as lipids or protein)

• Serum sodium Before embarking on other investigations for Hyponatraemia, consider whether the sample suffered from dilution by being was taken near the site of an infusion, or whether there is any chance of laboratory error. If necessary, repeat the test.
• Serum potassium If raised, consider Addison's.
• Plasma Osmolality
  • Normal - (280 to 300 mOsmol/kg) consider pseudoHyponatraemia.
  • Increased - (>300 mOsmol/kg) likely to be due to hyperglycaemia.
  • Low - (<280 mOsmol/kg) further investigation depends on whether urine sodium is high or low (see Table 1).
• Urine sodium level If this is >20mmol/l a renal cause should be sought.
• Imaging Imaging may be contributory in some clinical situations. For example a chest X-ray may be required in suspected congestive cardiac failure, or a CT brain scan in patients with confusion or altered consciousness.

No treatment for mild Hyponatraemia is usually needed. Correct underlying cause (e.g. stop thiazide).
In symptomatic or severe form:

• Hypovolaemic Volume replacement with isotonic saline is required (intravascular volume expanders to raise blood pressure may be needed).
• Normovolaemic Fluid restriction to 500ml/24 hours should be instituted to achieve a serum sodium level of 130mmol/l. If this proves inadequate, demeclocycline should be used to induce partial nephrogenic diabetes insipidus (this may take 2 weeks to reach maximum effect). Alternatively, use furosemide + oral sodium chloride 3 g daily.
• Hypervolaemic - use furosemide ± ACE inhibitors ± water restriction to <1l/24 hours.

Too rapid correction of serum sodium can cause central pontine myelinolysis (also known as osmotic demyelination syndrome). This is caused by large shifts of intracellular water occurring outside the brainstem as well as in the pons. It is always associated with rapid correction to normal levels (therefore stop at 120mmol/l and allow more gradual correction subsequently). Symptoms occur 2-4 days later, typically with quadriplegia and pseudobulbar palsy but it can take the form of mutism with paralysis ('locked in' syndrome).