- As opposed to potassium which is intracellular.
Signs & Symptoms
- Diuretics (particularly thiazide & loop diuretics)
- Mineralocorticoid insufficiency (Addison’s)
- Osmotic dieresis (low glucose, urea)
- CNS disturbances – infection, neoplasm, vascular, inflammatory, trauma, psychosis
- Neoplasm – ectopic ADH secretion from SCLC (pancreas, head and neck)
- Pain – post abdominal and thoracic surgery
- Surgery – post transspehnoidal pituitary surgery in 20-35%
- Pulmonary disease – especially pneumonia
- Drugs – SSRI, carbamazepine, cyclophosphamide, opiates, MAOI, ECSTASY (can also be associated with excessive water intake).
Primary polydipsia – often seen in patients with psychiatric conditions esp. those in anit-psychotics. Also seen in those with lesions in hypothalamic thirst centre e.g. in sarcoidosis.
Low dietary Na+
Advanced renal failure – inability of the kidneys to excrete free water. Minimum urine osmolality can rise to 200mosm/kg despite no ADH. Low osmolality can be offset by increase urea. However as urea can cross freely across cell membranes, it is an ineffective osmole hence effective osmolality is decreased.
Hormonal insufficiency –
- History – fluid loss, excessive water intake, malignancy, addisons, hypothyroid
- Examination – oedema, extracellular water depletion
- Investigations – serum osmolality (275-290), urine osmolality, urine Na+
- Treat underlying cause
- Fluid restriction – below urine output. Used for oedematous states (heart and liver failure), SIADH, primary polydipsia and advanced renal failure
- Na+ replacement – true volume depletion (removes stimulus for ADH release) or adrenal insufficiency (replaces Na+ lost from kidneys)
- ADH antagonist