SIADH

• Syndrome of inappropriate antidiuretic hormone secretion is characterised by excessive secretion of antidiuretic hormone (ADH) from the posterior pituitary gland or another source
• ADH controls water reabsorption but not the retention of solutes. By increasing water retention, ADH assists in the dilution of the blood - decreasing the concentration of solutes such as sodium
• In SIADH there is a lack of an effective negative feedback mechanism - results in continual ADH production, independent of serum osmolarity

  This leads to abnormally low serum sodium levels and high urinary sodium levels
• Causes of SIADH:

  • Primary brain injury
  • Malignancy - small cell cancer releasing ADH
  • Drugs - carbamazepine, SSRIs and amitriptyline
  • Infectious - atypical pneumonia
  • Hypothyroidism
• Symptoms of SIADH:

  • Mild hyponatraemia - nausea, vomiting, headache, anorexia and lethargy
  • Moderate hyponatraemia - muscle cramps, weakness, confusion and ataxia
  • Severe hyponatraemia - drowsiness, seizures and coma
• Patients with SIADH are typically euvolemic or hypervolaemic - fluid overload and not dehydrated

  Signs: pulmonary oedema, peripheral oedema, raised JVP and ascites
• Investigations for SIADH:

  • U&Es - serum sodium low
  • Plasma osmolality - reduced
  • TFTs - hypothyroidism a potential cause
  • Serum cortisol - to rule out addison's disease as a cause of low sodium
  • Urine osmolality - raised despite low plasma osmolality
  • urine sodium - raised despite low serum sodium concentration
• The following features must be present for a diagnosis of SIADH to be established:

  • Hyponatraemia
  • Low plasma osmolality
  • Inappropriately elevated urine osmolality (i.e. greater than plasma osmolality)
  • Urine [Na+] >40 mmol/L despite normal salt intake
  • Euvolaemia
  • Normal thyroid and adrenal function
• Definitive management of SIADH is to treat the underlying cause

  Fluid restriction is a common management strategy to increase sodium

  If patients have acute symptomatic hyponatraemia they should receive IV hypertonic saline
• If SIADH is suspected, consider a CT TAP and head
• CNS causes:

  • Stroke
  • SAH
  • Trauma
  • Psychosis
• Hormonal causes:

  • Hypothyroidism
  • Hypopituitarism
• Hypothyroidism causes SIADH due to reduced cardiac output and reduced renal blood flow which causes release of ADH
• Signs of SIADH:

  • Seizures
  • Reduced GCS
  • Coma
  • Myoclonus
  • Ataxia
  • Hyporeflexia
  • Asterixis
• Rapid increases in plasma sodium may result in osmotic demyelination syndrome - due to a rapid increase in extracellular osmolality. It can cause irreversible neurological damage.
• A newer class of drugs termed vaptans (e.g. tolvaptan) are now more commonly used. These vasopressin receptor antagonists are effective but expensive agents.
• Those with severe hyponatraemia are at risk of permanent neurological damage due to cerebral oedema, typically seen following a rapid (< 48 hrs) drop in sodium to below 120 mmol/L.