Hyponatraemia

Sodium levels are very closely linked to fluid levels, as sodium is an extracellular electrolyte.
  • As opposed to potassium which is intracellular.

Signs & Symptoms

Neurological:

Classification

Hypovolaemic hyponatraemia

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

GI

Other

Euvolaemic Hyponatraemia

Sodium levels are usually quite near to normal

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

Hypervolaemic Hyponatraemia

The high blood volume occurs due a high concentration of some other solute in relation to sodium.
Diagnosis:
  • History – fluid loss, excessive water intake, malignancy, addisons, hypothyroid
  • Examination – oedema, extracellular water depletion
  • Investigations – serum osmolality (275-290), urine osmolality, urine Na+
Management:
  • Treat underlying cause
  • Fluid restriction – below urine output. Used for oedematous states (heart and liver failure), SIADH, primary polydipsia and advanced renal failure
  • Na+ replacement – 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. 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 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

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