What is hyponatraemia?

What is hyponatraemia?

Hyponatraemia means a low sodium level in the blood. 

Sodium levels are very closely linked to fluid levels, as sodium is the primary extracellular electrolyte – as opposed to potassium which is intracellular.

Patients may be hypovolaemic (‘dry’), hypervolaemic (‘wet’) or euvolaemic (‘in the middle’).

Hyponatraemia is commonly seen both in the community (especially elderly patients, where it is very common, upto 30%) and in hospital – particularly in ICU (30%), geriatric, endocrine and renal wards.

Normal sodium level is 135-145 mmol/L.

So. What is hyponatraemia?

Definition of hyponatraemia

Can be considered by severity, and by type (related to fluid status):

Severity:

• Mild – 125 – 134 mol/L
• Moderate – 120-124 mmol/L
• Severe – <120 mol/L.

Types:

• Hypovolaemic
• Euvolaemic
• Hypervolaemic.

Hypovolaemic hyponatraemia

Typically due to excess sodium loss.

The low blood volume is usually a result of the low sodium. The reduction in sodium is usually relatively greater than the reduction of fluid volume.

Causes:

• Renal
  • Diuretics (particularly thiazide & loop diuretics)
  • Mineralocorticoid insufficiency (Addison’s)
  • Osmotic diuresis (low glucose, urea)
• GI
  • Vomiting or diarrhoea
  • Pancreatitis
  • Bowel obstruction
  • Peritonitis
• Other
  • Burns
  • Rhabdomyolysis
  • Excessive sweating
• Bleeding.

Euvolaemic hyponatraemia

Typically due to water excess. Sodium levels are usually quite near to normal (i.e. typically ‘mild’ – sodium of 125-134 mol/L).

Causes

• Diuretics
• SIADH (syndrome of inappropriate ADH secretion) = persistent release of ADH despite normovolaemia leading to water retention. Causes include:
  • CNS disturbances – infection, neoplasm, vascular, inflammatory, trauma, psychosis
  • Neoplasm – ectopic ADH secretion from SCLC (pancreas, head and neck)
  • Pain – post abdominal and thoracic surgery
  • Surgery – post trans-sphenoidal pituitary surgery (20-35%)
  • Pulmonary disease – especially pneumonia
  • Drugs – SSRI, carbamazepine, cyclophosphamide, opiates, MAOI, ECSTASY (can also be associated with excessive water intake)
• Primary polydipsia – often seen in patients with psychiatric conditions especially those on anti-psychotics. Also seen in those with lesions in hypothalamic thirst centre, e.g. sarcoidosis
• Low dietary Na+
• Advanced CKD (CKD4-5) – inability of the kidneys to excrete free water. Minimum urine osmolality can rise to 200 mosm/kg despite no ADH. Low osmolality can be offset by increase urea. However as urea can cross freely across cell membranes, it is an ineffective osmole hence effective osmolality is decreased.
• Hormonal insufficiency
  • Addison’s
  • Hypothyroidism
• Pregnancy – HCG ‘sets’ osmostat lower by 5 mmol/L.

Hypervolaemic hyponatraemia

Typically due to an increase in total body water and sodium, but they are not proportional. The high blood volume occurs due a high concentration of some other solute in relation to sodium.

Causes

• Chronic heart failure (CHF)
• Advanced CKD (CKD4-5)
• Nephrotic syndrome
• Liver failure
• GI failure (malabsorption or malnutrition).

Symptoms

May be none if hyponatraemia is mild.

• Neurological
  • Confusion
  • Lethargy
  • Seizures
  • Coma
  • Headaches
• Other: muscular weakness

History

The speed of onset is a critical factor in the history – rapid onset is more likely to result in significant sequelae. Patients are typically not symptomatic until sodium <125 mmol/L.

Examination

• GCS
• Assessing volume status clinically is unreliable, but still should be attempted:
  • Moist or dry mucus membranes
  • Signs of fluid retention
  • Weight loss / gain
  • JVP.

Note. A more sensitive method is to look at serum urea and urinary Na+. A low or normal urea in conjunction with elevated urinary Na+ makes normovolaemic hyponatraemia more likely.

Investigation

• U+E (sodium and renal function)
• Glucose
• Plasma and urinary osmolality (normal plasma level 275-290), normal urine level 3x greater than plasma level
• Urinary Na+ – 15-250mmol/L is normal.

Treatment

1. Treat the underlying cause

2. Correct the fluid state

3. Correct sodium level slowly to avoid central pontine myelinolysis.

Common interventions include:

• Fluid restriction to 750 mls daily (or, at a minimum, to less than urine output) – use for hypervolaemic (oedematous) causes, SIADH, and primary polydipsia
• Cease any implicated medication
• Isotonic or hypertonic (3%) saline – if truly volume depleted (removes stimulus for ADH release) or adrenal insufficiency (replaces Na+ lost from kidneys)
• ADH antagonist (e.g. Tolvaptan).

Note. Avoid rapid correction of hyponatraemia – especially if severe (<115mmol/L). Replacing Na+ too quickly can lead to osmotic demyelination syndrome (aka central pontine demyelinosis). The brain compensates for hyponatraemia associated oedema within the first day and is complete within a few days.

Replacing Na+ too quickly leads to fluid being drawn out of the CNS hence the brain goes from too much fluid to too little rapidly – causing demyelination. This occurs when Na+ replacement exceeds 10-12mmol/L/24hrs or 18mmol/L/48hrs. Hence aim to replace Na+ by <10mmol/L /24hrs and <18mmol/L/48hrs.

If acutely seizing:
Raise sodium by 1-5mmol/L/hour until stops seizing or sodium 125-130mmol/L, e.g with hypertonic saline (3%)

SIADH and asymptomatic:

• Fluid restriction
• Frusemide 20-40mg IV daily
• Oral NaCl tablets 3-18g daily
• Democlocycline 600-1200mg daily.

Prognosis (outlook)

The mortality of hyponatraemia is very variable, depending on its severity, and age of the patient as shown in this study: Hao, 2017.

This graph is taken from the paper. Severe hyponatraemia has an in-hospital mortality of 15-35% depending on the age of the patient. Patients usually die with it (i.e. of the cause of the hyponatraemia) rather than because of it.

Summary

We have described what is hyponatraemia; and focused on its causes, symptoms, treatment, and outlook. We hope it has been helpful.

Other resource

This is a review article: Rondon, 2023

 

Last Reviewed on 24 April 2024