Synopsis
Diagnose syndrome of inappropriate antidiuresis only after excluding mimics, treat neurological emergencies safely, and target the underlying driver of water retention.
- SIAD is a diagnosis of hypotonic hyponatraemia with inappropriately concentrated urine after effective-volume depletion, adrenal insufficiency, severe hypothyroidism, kidney failure and diuretics are addressed.
- Confirm true hypotonicity because hyperglycaemia, exogenous osmoles and pseudohyponatraemia create different physiology and treatment.
- Urine osmolality shows whether AVP activity is present; maximally dilute urine points towards excess intake rather than persistent antidiuresis.
- Interpret urine sodium with volume status, dietary intake, kidney function and recent diuretics; no single urine threshold proves SIAD in isolation.
- Common drivers include pulmonary disease, central nervous system disease, malignancy, pain, nausea, postoperative stress and medicines such as antidepressants or antiseizure drugs.
- Severe symptomatic hyponatraemia receives controlled hypertonic saline regardless of whether SIAD has yet been confirmed.
- For chronic stable SIAD, fluid restriction is often first-line, but likely response depends on electrolyte-free water clearance and ongoing obligatory intake.
- Tolvaptan, oral urea and other second-line strategies require specialist selection and local policy; tolvaptan can overcorrect and must never substitute for emergency hypertonic saline.
Investigation priorities
Confirm that low sodium represents hypotonic hyponatraemia rather than a non-hypotonic state.
Management branches
Hypotonic hyponatraemia accompanies seizure, reduced consciousness or another severe neurological syndrome.
- Begin monitored ABCDE care, check glucose, stop hypotonic fluid and obtain serum and urine samples if this causes no treatment delay.
- Give protocol-defined boluses of hypertonic saline, reassessing symptoms and sodium after each rather than prescribing an open-ended infusion.
- Set correction limits, monitor urine output and sodium frequently, involve critical care or endocrinology, and use a specialist reversal plan if the rise becomes excessive.
Stable hypotonic hyponatraemia has no immediately obvious volume-depleted or oedematous cause.
- Review onset, fluid and solute intake, examination, medicines, renal function, glucose and paired serum and urine osmolality with urine sodium.
- Exclude cortisol deficiency and clinically relevant thyroid or kidney disease, accounting for recent diuretic exposure and treatment already given.
- Search proportionately for a pulmonary, neurological, malignant, postoperative or pharmacological driver and label SIAD only when the physiology coheres.
Key medicines
Hypertonic sodium chlorideAdminister the current Society for Endocrinology protocol-defined bolus in a monitored acute setting, repeat only after symptom and sodium reassessment, and stop when the limited initial correction goal is achieved.It is not routine treatment for asymptomatic chronic SIAD. Overcorrection risks osmotic demyelination; verify concentration, use controlled administration, account for potassium and spontaneous aquaresis, and have a reversal plan.
TolvaptanInitiate only under an experienced specialist and local commissioned protocol at the approved starting regimen, with free access to water and closely timed sodium checks; adjust according to response rather than routine escalation.Can cause thirst, dehydration and dangerously rapid sodium correction, particularly when baseline sodium is low or SIAD resolves. It is not emergency therapy and requires liver, interaction and licence review.