Question 7

List the causes of hyponatraemia in the intensive care patient  population, and outline your management of hyponatraemia.

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College Answer

Causes are numerous. Lists should include:
Factitious: contaminated by hypotonic intravenous fluid
Isotonic: pseudohyponatraemia [hyperlipidaemia, hyperproteinaemia] Hypertonic: eg. hyperglycaemia, mannitol
•    water retention: SIADH, inappropriate antidiuresis [eg. hypovolaemia, cardiac failure, pain, post-operative, renal failure], psychogenic polydipsia, TURP syndrome
•    salt depletion: adrenocortical failure, diuretic excess

Management includes diagnosis and, if appropriate, specific treatment of underlying cause. Most patients are asymptomatic, with plasma Na > 120. Initial treatment with water restriction and isotonic saline is usually sufficient. More aggressive therapy (eg. hypertonic saline) is indicated if Na < 110, or if patient is symptomatic (eg. confusion, coma, seizures). Relationship of rate of correction of Na and risk of osmotic demyelination (central pontine myelinolysis) is controversial, but appears reduced if rate of correction of Na is less than 10-12 mmol/L (ie. :S 0.5 mmol/hr). Desmopressin (dDAVP) may be required to slow the rate of water excretion. Consider even administration of sterile water to lower sodium if rising too quickly.


This question closely resembles Question 14 from the first paper of 2005.

The answer to it is reproduced below:

Potential causes:

This is essentially the content of Box 93.1 from Anthony Delaney and Simon Finfer's chapter for Oh's Manual.

Causes of Hyponatremia

Spurious result


  • High triglycerides
  • High serum protein
  • Glycine (TURP syndrome)


  • Hyperglycaemia
  • Mannitol
  • Sorbitol
  • Maltose
  • Radiocontrast dye

Water retention

High urine sodium

  • Renal failure
  • Cirrhosis
  • Congestive cardiac failure
  • Diuretics (but not enough!)

Low urine sodium

  • Psychogenic polydipsia
  • True hypovolemia

Sodium excretion

  • Post-ATN diuresis
  • Hypoaldosteronism
  • Diuretic excess
  • Cerebral salt wasting
  • Inappropriate fluid replacement (5% dex)

Diagnosis on the basis of the above lab tests and historical findings:


The following bits of historical information are important:

  • Medication history (diuretics, steroids, drugs which cause SIADH eg. SSRIs)
  • Fluid chart (has somebody been mindlessly charting dextrose)
  • Psychosocial history (is psychogenic polydipsia even a possibility; are they on a weird diet)
  • Alcohol history (liver disease, cirrhosis, beer potomania)
  • Oedema history (Ascites worse recently? Sleep on twenty pillows?)
  • Trauma history (cerebral salt wasting, pituitary injury)
  • Urine output (massive diuresis of HONK or ATN recovery phase, or oliguria or chronic renal failure)
  • Recent procedures: TURP, contrast CT, recent surgery, etc.

The following standard battery of tests can be launched; particularly if history is unhelpful, or one cannot bring oneself to interview the patient or their family.

  • Serum osmolality testing:
    • Hyperosmolar hyponatremia:
      • Hyperglycaemia
      • Mannitol therapy
      • Other unmeasured solutes, eg. glycine
      • Glycine (TURP syndrome)
    • Isoosmolar hyponatremia
      • High triglycerides
      • High serum protein
    • Hypoosmolar hyponatremia
      • Further investigations will be required to distinguish between water retention and sodium excretion.
  • Urinary sodium and urinary osmolality
    • Low urinary sodium: water retention disorders;
      • Polydipsia, beer potomania - low urine osmolality
      • true hypovolemia, heart failure, cirrhosis, nephrotic syndrome - high urine osmolality
    • High urinary sodium: sodium wasting disorders;
      • Acute renal failure, post-obstructive diuresis, polyuric phase of ATN - low urine osmolality
      • Thiazides, SIADH, cerebral salt wasting, hypoadrenalism, hypothyrodism - high urine osmolality


  • Reverse the reversible causes
  • Restore volume and sodium with isotonic saline (if appropriate)
  • If there are severe symptoms, hypertonic saline infusion is required.
  • Sodium replacement rate should not excess 12mmol/day, or about 0.5mmol/hr.


Lazaridis, Christos, et al. "High-Osmolarity Saline in Neurocritical Care: Systematic Review and Meta-Analysis*." Critical care medicine 41.5 (2013): 1353-1360.

Adrogué, Horacio J. "Consequences of inadequate management of hyponatremia." American journal of nephrology 25.3 (2005): 240-249.

Froelich, Matteus, et al. "Continuous hypertonic saline therapy and the occurrence of complications in neurocritically ill patients*." Critical care medicine 37.4 (2009): 1433-1441.

R J Martin Central pontine and extrapontine myelinolysis: the osmotic demyelination syndromes J Neurol Neurosurg Psychiatry 2004;75:iii22-iii28 doi:10.1136/jnnp.2004.045906

For all electrolyte abnormality questions, I refer to the Electrolyte Quintet series from the Lancet. In the sodium article by Kumar, there is a table (Panel 2) from which the college answer seems to be derived (with a couple of changes). I have used that panel as my model answer.

Sumit Kumar, Tomas Berl. Sodium.  The LancetVolume 352, Issue 912318 July 1998Pages 220-228

Laureno, Robert, and Barbara Illowsky Karp. "Myelinolysis after correction of hyponatremia." Annals of Internal Medicine 126.1 (1997): 57-62.

Lee, Eun Mi, et al. "Risk factors for central pontine and extrapontine myelinolysis following orthotopic liver transplantation." European neurology 62.6 (2009): 362-368.

Adams, Raymond D., MAURICE VICTOR, and ELLIOTT L. MANCALL. "Central pontine myelinolysis: a hitherto undescribed disease occurring in alcoholic and malnourished patients." AMA Archives of Neurology & Psychiatry 81.2 (1959): 154-172.

Brown, William D. "Osmotic demyelination disorders: central pontine and extrapontine myelinolysis." Current opinion in neurology 13.6 (2000): 691-697.

Harris, Cheryl P., J. J. Townsend, and J. Richard Baringer. "Symptomatic hyponatraemia: can myelinolysis be prevented by treatment?." Journal of Neurology, Neurosurgery & Psychiatry 56.6 (1993): 626-632.