College Answer

Causes are numerous. Lists should include:
Factitious: contaminated by hypotonic intravenous fluid
Isotonic: pseudohyponatraemia [hyperlipidaemia, hyperproteinaemia] Hypertonic: eg. hyperglycaemia, mannitol
Hypotonic:
•    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.

Discussion

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.

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

History

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

Treatment:

• 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.