Hyponatraemia (serum Sodium <135 mmol/L) is one of the most common electrolyte abnormalities you will see and so a systematic approach to identifying the underlying cause and management is vital. We will use the algorithm below from ESE which is far easier to use than the antiquated system of first assessing their volume status.

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Recommended Investigations

• Serum & urine osmolality, urinary sodium
• If fluid overloaded: BNP, liver tests, U&Es, urine dip & protein-creatinine ratio
• Endocrinopathy screen: TFTs, 9am cortisol (random if adrenal insufficiency highly suspected)

Recommended Steps (whilst awaiting investigations)

• Consider false hyponatraemia (below) due to hyperglycaemia
• Take a thorough fluid input/output history (including alcohol)
• Consider recent surgery (transient & usually self corrects)
• Stop non-essential medications that could be contributing (e.g. PPIs, diuretics if not overloaded, ACE/ARBs)
• Restrict fluids if oedematous (750ml to 1L / 24 hours)
• Give 1L 0.9% sodium chloride IV if non-oedematous (as SIADH is rare & it is difficult to differentiate euvolaemia from mild hypovolaemia)

False Hyponatraemia

• Normal plasma osmolality is 275-295 mOsmol/kg. In patients with hyponatraemia, the serum osmolality should be low. This is because sodium is the main osmole so if it is low, so should the serum osmolality.
• If it isn’t low, consider whether it is falsely lowered due to interfering glucose, lipids or proteins.
• Of these, glucose is by far the most common & it is simple to calculate the corrected sodium. Use this calculator for every patient with significant hyperglycaemia.
• Thus, a patient with a sodium of 129 & blood glucose of 28 actually has a normal corrected sodium.
• Furthermore, a patient with a sodium of 140 & blood glucose of 35 actually has hypernatraemia.

Severity of Hyponatraemia

Severe Hyponatraemia

This may require urgent correction when the sodium is ≤120 with vomiting, reduced GCS, seizures or cardiorespiratory distress.

Overall it is rare to have severe hyponatraemia causing symptoms as the brain rapidly adapts (≤48 hours) to the lower osmolality. With the brain used to this lower osmolality, rapid correction with hypertonic saline can lead to dangerous neurological consequences like osmotic demyelination. It may be necessary though to use hypertonic saline if the above life-threatening symptoms are occurring.

Overall, it is safer to assume the patient does NOT have severe symptomatic hyponatraemia & that the neurological or cardiorespiratory features are caused by something else due to the risk of osmotic demyelination.

Chronic severe hyponatraemia (>48 hours) can lead to gait instability, falls & cognitive impairment. As in moderate hyponatraemia, apply the algorithm below.

Low Urine Osmolality (≤100)

There is very dilute urine due to either too much fluid or too little salt. Therefore causes include primary polydipsia, low solute intake, beer potomania which can be identified with a thorough history. Management is fluid restriction 750 ml to 1L/24 hours with slow sodium 2 tablets QDS.

Raised Urine Osmolality (>100)

Low Urinary Sodium (≤30)

Low urinary sodium is an appropriate response to hyponatraemia (i.e. the body is conserving sodium) due to the renin-angiotensin-aldosterone system & ADH being secreted which conserves water (diluting the sodium further). The body releases these hormones whenever it senses the circulating volume and/or pressure isn’t quite right.

This may occur in patients with heart failure, liver cirrhosis or nephrotic syndrome which should be identifiable from the presence of peripheral oedema and/or blood tests (raised BNP, deranged LFTs or protein-creatinine ratio/U&Es respectively). In these situations, fluid restriction to 750 ml to 1L/24 hours and/or diuresis will correct the “too much water” problem.

It also occurs when the patient is volume deplete, either due to D&V, third spacing or remote (“recently used”) diuretics. In this case, treatment with 0.9% sodium chloride will correct this.

High Urinary Sodium (>30)

This is an inappropriate response as the kidneys are excreting sodium when they shouldn’t be. This is usually due to kidney dysfunction, diuretics or endocrine dysfunction. It is often helpful to request an endocrinology review. It is vital that you rule out any endocrinopathies before considering SIADH.

Differentiating between euvolaemia & hypovolaemia can be difficult. Postural hypotension is a much more sensitive way to pick up subtle hypovolaemia. Strongly consider whether adrenal insufficiency may be the underlying aetiology – the postural hypotension and random or 9 am cortisol will be helpful to identify this. If diagnosed, IV fluids & hydrocortisone 50 mg IV QDS will help treat this.

SIADH

Diagnostic criteria include

• Low serum osmolality, high urine osmolality (>100) & high urinary sodium (>30)
• No recent diuretic usage or kidney dysfunction
• No endocrinopathy (pituitary, adrenal or thyroid dysfunction)
• Failure to correct sodium with 0.9% sodium chloride (may cause transient increase lasting <24 hours)
• Sodium corrected by fluid restriction

Causes includes

• Brain: injury, tumour or infection
• Drugs: antiepileptics, antidepressants, PPIs
• Malignancy: particularly lung cancer
• Respiratory infections

Treatment includes

• Very strict fluid restriction to 750 ml to 1L / 24 hours
• Fluid restriction is very often poorly adhered to because water jugs are regularly filled, cups of tea, food/drink. If the sodium isn’t increasing, check the fluid restriction
• Other treatments may include oral urea, slow sodium

Resources & References

• ESE Hyponatraemia Guidelines
• UpToDate on Hyponatraemia
• BMJ Best Practice
• Biswas M, Davies JS. Hyponatraemia in clinical practice. Postgrad Med J. 2007;83(980):373–378. doi:10.1136/pgmj.2006.056515
• National Institute for Health and Care Excellence. Hyponatraemia. Retrieved from https://cks.nice.org.uk/hyponatraemia#!topicSummary
• Allen J, Newland-Jones P. How to manage adults with hyponatraemia. Clinical Pharmacist, Vol. 4, p262 | URI: 11108156

Written by Dr Akash Doshi (Endocrinology ST3) & Dr Angela Yan (FY2)