The Syndrome of Inappropriate Antidiuretic Hormone (SIADH) secretion is defined by a combination of hyponatremia and hypo-osmolality arising from one of the following:

  • Excess ADH release from the hypothalamus/pituitary. This can follow brain injury (traumatic, anoxic, haemorrhagic or inflammatory), stroke or neurological tumours. It is less frequently associated with other neurological disorders.
  • Excess ADH production in ectopic sites. Inflammatory conditions or tumours in extracranial sites can be associated with abnormal ADH production. This is particularly likely with respiratory inflammatory disorders or lung tumours.
  • Excess ADH production or renal sensitivity to ADH can be triggered by specific medications, especially opiates, NSAIDs, anticonvulsants, antidepressants, antipsychotics, hypoglycemic agents and anticancer drugs (anti-neoplastic agents).

NOTE: If patients have persisting SIADH, then other causes need to be considered. Consult your employing health authority’s specific management protocols for investigation and management of this condition.

In SIADH the trigger for hyponatraemia arises from reduced water loss in the kidneys. Thus it is a condition of excess total body water rather than reduced body sodium. Therefore treatment is aimed at reducing total body water.

Bartter-Schwartz Syndrome is characterised by excessive release of antidiuretic hormone from the posterior pituitary gland or another source. The Criteria for the diagnosis of Bartter-Schwartz are:

  • Hyponatraemia (Serum sodium < 135 mmol/l) with corresponding serum hypo-osmolality(< 280 mOsm/l).
  • Continued renal excretion of sodium:
    • Urinary sodium > 30mmol/l
    • Which is inappropriate in context of hyponatraemia.
  • Urine less than maximally dilute:
    • Urine osmolality >100
    • Which is inappropriate in context of serum hypo-osmolality.
  • Absence of clinical evidence of volume depletion.
  • Absence of other causes of hyponatraemia.
  • Correction of hyponatraemia in response to fluid restriction. If fluid restriction does not correct hyponatraemia, then you need to reconsider the diagnosis.

If the SIADH is persistent or difficult to treat then you need to review the possible causes. In particular consider the possibility of Cerebral Salt-Wasting however also consider other possible causes of SIADH and hyponatraemia. In addition to the investigations above you should include investigations such as:

  • Medication review.
  • Chest radiography looking for respiratory causes.
  • CT or MRI of the head looking for neurological causes.
  • Uric acid, liver function and endocrine screening.

Treatment of SIADH
Over-rapid correction of hyponatremia may lead to potential neurological complications, in particular central pontine myelinolysis (a demyelinating condition of the pons). General principles of treatment depend on the rapidity of onset and severity of the clinical features/hyponatraemia. Treatment options include:

  • Identify cause and treat.
  • Fluid restriction.
  • Intravenous saline administration
  • Medication options include mannitol; demeclocycline or loop diuretics.

NOTE: You should seek senior medical advice or consult your employing health authority’s specific management protocols for investigation and management of this condition.