SIADH 

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) Summary: 

• can occur secondary to medications, malignancy, pulmonary disease, or any disorder involving the central nervous system. 
• Diagnosis is made on the basis of clinical euvolaemic state with low serum sodium and osmolality, raised urine sodium and osmolality, and exclusion of pseudohyponatraemia and diuretic use. 
• Fluid restriction of 800–1200 mL/24 hours is the mainstay of treatment
• Patients with severe hyponatraemia and symptoms of altered mental state or seizures should be admitted to hospital for monitoring of fluid restriction and consideration of hypertonic saline. A rapid increase in sodium levels can precipitate osmotic demyelination and, as such, the increase in serum sodium should not exceed 10 mmol/L in 24 hours or 18 mmol/L in 48 hour

Pathology

• In SIADH, hyponatraemia is due to inappropriate secretion of antidiuretic hormone (ADH). 
• In a normal physiological state, ADH is released in response to increased serum osmolality, whereas in SIADH, ADH secretion is unregulated.
•  Increased production/ectopic production or increased sensitivity to ADH results

🡪  in increased water permeability of the renal distal tubule and collecting duct through aquaporin insertion.

• The subsequent dilutional hyponatraemia activates volume-sensitive natriuretic mechanisms, causing salt excretion and maintaining euvolaemic hyponatraemia

Underlying causes of SIADH

• Neurosurgical or neurological – increased ADH release:
  • Guillain-Barré syndrome
  • Subarachnoid haemorrhage
  • Subdural haemorrhage
• Infective – increased ADH release:
  • Meningitis
  • Encephalitis
  • Abscesses
  • Human immunodeficiency virus
  • Sarcoidosis
• Respiratory – increased ADH release:
  • Tuberculosis
  • Pneumonia
  • Pneumothorax
  • Atelectasis
  • Asthma
• Medications – increased ADH release:
  • Antidepressants (eg sertraline)
  • Anticonvulsants (eg carbamazepine, leveteiracetam)
  • Antipsychotics (eg haloperidol)
  • Anti-inflammatory drugs
  • Ecstasy
  • Cyclophosphomide
• Malignancy – ectopic ADH production:
  • Nasopharyngeal
  • Mesothelioma
  • Pancreatic
  • Gastrointestinal
  • Lymphoma
  • Sarcoma

Diagnosis of SIADH

• decreased serum osmolality (<275 mOsm/kg)
• increased urine osmolality (>100 mOsm/kg)
• euvolaemia
• increased urine sodium (>20 mmol/L)
• no other cause for hyponatraemia (no diuretic use and no suspicion of hypothyroidism, cortisol deficiency, marked hyperproteinaemia, hyperlipidaemia or hyperglycaemia).

Investigations for underlying causes

• biochemistry looking at serum sodium level
• serum osmolality
• urine osmolality (random sample collected at same time as serum sample)
• thyroid function tests
• morning cortisol level if hyponatraemia is potentially related to Addison’s disease
• computed tomography (CT) of the head if a neurosurgical condition is suspected (eg subarachnoid haemorrhage, subdural haematoma)8
• chest X-ray if pulmonary causes of SIADH are suspected.

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