Hyponatraemia and Syndrome of Inappropriate Antidiuretic hormone production (SIADH)

Background

• Hyponatraemia is the most common electrolyte disturbance encountered.  Up to 30% of hospitalised patients will be hyponatraemic.  SIADH is the most common cause.
• Usually asymptomatic but can manifest as anorexia, nausea, vomiting, confusion, lethargy, seizures and coma.
  • Severity of symptoms are usually representative of the rate of change rather than the severity of change (chronic hyponatraemia is rarely symptomatic)

Classifications of hyponatraemia

• Hypovolaemic (sodium deficit with a relatively smaller water deficit)
  • e.g. renal sodium loss; diuretic therapy (esp thiazide diuretics); adrenocortical failure (e.g. Addison’s disease); GI sodium losses (diarrhoea/vomiting); burns
    • i.e. cause is often apparent (except perhaps in Addison’s/hypoadrenalism)
  • may have features of hypovolaemia e.g. thirst, dizziness, weakness, dry mucous membranes, reduced urine output etc
• Euvolaemic (water retention alone)
  • Polydipsia; excessive electrolyte-free (e.g. 5% dextrose solution) infusions; SIADH (see below); hypothyroidism
• Hypervolaemic (sodium retention with relatively greater water retention)
  • Congestive heart failure; cirrhosis; nephrotic syndrome; chronic renal failure

SIADH

Physiology

• During resting states (normal homeostasis)- ADH is produced in the hypothalamus and stored in the posterior pituitary
• Osmoreceptors in the hypothalamus detect changes in the ECF osmolality (most commonly as a result of serum sodium concentrations)
• In the hyperosmolar state, they stimulate ADH secretion.  In the hypoosmolar state, they result in decreased production of ADH.
• The action of ADH is primarily renal: increasing the number of aquaporin receptors in the collecting tubule, allowing for a greater reabsorption of water and dilution of the blood i.e. lower sodium concentration is actually due to higher ECF water content than actual number of moles of sodium
• SIADH is characterised by
  • hyponatraemia
  • inappropriately elevated urine osmolality (>100mmol/kg) (can be higher than plasma osmolality)
  • excessive urine sodium concentrations (>30mmol/l)
  • decreased serum osmolality (<270mmol/kg)
  • in a euvolaemic patient, with no evidence of renal, cardiac or hepatic disease potentially associated with hyponatraemia

Causes

• Tumours
• CNS disorders e.g. stroke, trauma, infection, psychosis, porphyria
• Pulmonary disorders: pneumonia, tuberculosis, obstructive lung disease
• Drugs: anticonvulsants; psychotropics; antidepressants; cytotoxics; oral hypoglycaemics; opiates
• Idiopathic

Investigations

• Plasma and urine electrolytes/osmolaltiy
  • NB U&Es should be measured more than once in case of false positives
    • Low Na
    • Potassium- can be raised in Addison’s
• Imaging can be useful e.g. CXR in heart failure

 

Management

• Correct any underlying cause e.g. stop diuretic
  • Beware of correcting too rapidly- particularly in chronically hyponatraemic patients (no more than 8-10 mmol/l/day)
    • can cause myelinolysis (demyelination)
• If hypovolaemic- fluid replacement (0.9% saline)
  • NB beware of subsequent diuresis and rapid conversion to hypernatraemia (if this occurs, give desmopressin (ADH analogue) and 5% glucose (water))
• If normovolaemic/hypervolaemic
  • Fluid restrict (500-1000ml/day)
    • Consider adding furosemide if symptomatically hypervolaemic
    • Consider adding NaCl tablets/3% saline if the urine osmolality exceeds that of plasma
• NB If also hypokalaemia, potassium will raise both K and Na in the serum.