Sodium and Hyponatraemia

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Contents

Introduction
Hyponatraemia
References
Related Articles

Introduction

Sodium levels are very closely linked to fluid levels, as sodium is an extracellular electrolyte.

As opposed to potassium which is intracellular.

Hyponatraemia is commonly seen both in the community (especially older patients) and in hospital – particularly in ICU – where 30% of patients have hyponatraemia.

Normal sodium level is 135-145mmol/L

Hyponatraemia

Can be considered by severity, and by cause:

Severity:

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

Types:

Hypovolaemic
Euvolaemic
Hypervolaemic
Iso-osmolar
Hypertonic

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.

Renal causes:

Diuretics (particularly thiazide & loop diuretics)
Mineralocorticoid insufficiency (Addison’s)
Osmotic dieresis (low glucose, urea)
Nephropathy

Vomiting
Diarrhoea
Pancreatitis
Bowel obstruction
Peitonitis

Other

Burns
Rhabdomyolysis
Excessive sweating
Bleeding

Euvolaemic Hyponatraemia

Sodium levels are usually quite near to normal (i.e. typically “mild” – sodium of 125-134 mol/L)

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 transspehnoidal pituitary surgery in 20-35%
Pulmonary disease – especially pneumonia
Drugs – SSRI, carbamazepine, cyclophosphamide, opiates, MAOI, ECSTASY (can also be associated with excessive water intake).
Idiopathic

Primary polydipsia – often seen in patients with psychiatric conditions esp. those in anit-psychotics. Also seen in those with lesions in hypothalamic thirst centre e.g. in sarcoidosis.

Low dietary Na⁺

Advanced renal failure – inability of the kidneys to excrete free water. Minimum urine osmolality can rise to 200mosm/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

There is a total body increase in 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.

Heart failure
Renal failure – particularly nephrotic syndrome
Liver failure
Hyperglycaemia

Signs & Symptoms

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.

Fluid intake / output – is it related to excess fluid intake ror excessive fluid loss – e.g. due to malignancy, addisons, hypothyroidism
Nausea / vomiting – vomiting can cause a hypovolaemia hyponatraemia
Muscular weakness
Confusion
Psychosis
Medications – particularly diuretics, SSRI and PPI – especially if any recent changes

Examination

GCS
Volume status (see below)

Assessing volume status

Assessing volume status clinically is unreliable, but still should be attempted:

Moist or dry mucus membranes
Signs of fluid retention
Weight loss / gain
JVP

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.

Investigations

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

Management

Treat the underlying cause
Correct sodium level slowly to avoid central pontine myelinolysis
Common interventions include:
- Fluid restriction to 800mls daily (or at minimum to less than urine output) – Used for oedematous states (heart and liver failure), SIADH, primary polydipsia and advanced renal failure
- Cease any implicated medications
- Isotonic or hypertonic (3%) saline – if true volume depletion (removes stimulus for ADH release) or adrenal insufficiency (replaces Na⁺ lost from kidneys)
- ADH antagonist

Avoid rapid early correction of hyponatraemia, especially 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

Targets

If acutely seizing:
- Raise sodium by 1-5mmol/L/hour until stops seizing or sodium 125-130mmol/L
- Hypertonic saline (3%)
- Consider frusemide 20mg IV
If symptomatic but chronic (>48 hours), not actively seizing
- Aim to raise sodium by 10mmol/24hours
SIADH and asymptomatic
- Fluid restriction
- Frusemide 20-40mg IV daily
- Oral NaCl tablets 3-18g daily
- Urea 30g daily
- Democlocycline 600-1200mg daily