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Hyponatraemia

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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.

Epidemiology

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

Presentation1

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

Syndrome of Inappropriate Anti-Diuretic Hormone Secretion (see SIADH)
The normal mechanism that controls homeostasis (stimulation of ADH secretion in response to low plasma volume or high osmolality) can be over-ridden in certain situations causing SIADH. There are a large number of causes including neurological disease, pulmonary disease, malignancy, and drugs. Diagnosis requires presence of all following criteria:

  • 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
Causes1,4

The causes of Hyponatraemia can be divided into three groups:

  • Hypovolaemic
  • Normovolaemic
  • Hypervolaemic

Table 1- Causes and Diagnosis of Hyponatraemia

Key Question: Is the patient hypovolaemic (dehydrated)?

YES? (Hypovolaemic) NO?
Is urinary sodium >20 mmol/l? Does the patient have signs of oedema?
YES? NO? NO? (Normovolaemic) YES? (Hypervolaemic)
Sodium and water are being lost through the kidneys:
Sodium and water are being lost elsewhere:
Is urine osmolality >100 mOsmol/kg?

Yes
SIADH

No

  • Water overload
  • Excess 5% dextrose
  • Severe hypothyroidism
  • Glucocorticoid deficiency
Primary polydypsia
Nephrotic syndrome
Cardiac failure
Cirrhosis
Renal failure
Differential Diagnosis1
  • 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)
Investigations
  • 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.
Management

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.

NB: whatever the cause, chronic, severe Hyponatraemia (Na <120mmol/l for more than 3 days) must be corrected slowly, i.e. at <0.5mmol/l/hour. Avoid an infusion of hypertonic saline if possible (seek expert help) - but if essential, increase serum sodium by <0.5mmol/l/hour (10mmol/l/24 hours) and stop infusion at 120mmol/l. Following formula may help:
Rate of infusion of 3% NaCl (ml/hour) = body weight (kg) x desired rate of correction (mmol/l/h).
If the Hyponatraemia has only occurred in the last 3 days and is causing acute symptoms (with drowsiness, convulsions or coma) it can be corrected more quickly - increase serum sodium by 2mmol/l/hour but stop at 120mmol/l. This condition is usually caused by giving large quantities of 5% dextrose infusion.

Complications

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).


Document references
  1. Craig S; Hyponatremia eMedicine.com 2008.
  2. Ellis SJ; Severe hyponatraemia: complications and treatment. QJM. 1995 Dec;88(12):905-9. [abstract]
  3. Bagshaw SM, Townsend DR, McDermid RC; Disorders of sodium and water balance in hospitalized patients. Can J Anaesth. 2009 Feb;56(2):151-167. Epub 2008 Dec 31. [abstract]
  4. Goh KP; Management of hyponatremia. Am Fam Physician. 2004 May 15;69(10):2387-94. [abstract]
Acknowledgements EMIS is grateful to Dr Laurence Knott for writing this article. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2009.
Document ID: 2298
Document Version: 23
Document Reference: bgp1101
Last Updated: 19 Mar 2009
Planned Review: 19 Mar 2011

The authors and editors of this article are employed to create accurate and up to date content reflecting reliable research evidence, guidance and best clinical practice. They are free from any commercial conflicts of interest. Find out more about updating.

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