SIADH
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Direct answer
Hypo-osmolar plasma with urine that refuses to dilute is the signature of SIADH: serum sodium under 135 mmol/L with plasma osmolality below 275 mOsm/kg, yet urine osmolality above 100 mOsm/kg (typically over 300) and urinary sodium above 30 mmol/L on normal salt and water intake, in a euvolaemic patient with normal thyroid, adrenal and renal function and no diuretic exposure. Small cell lung cancer is the textbook cause, but drugs (carbamazepine, SSRIs, cyclophosphamide, cisplatin), pneumonia, meningitis, stroke, nausea, pain and the postoperative state together account for far more hospital cases. Treatment is the underlying cause plus fluid restriction; severe symptomatic hyponatraemia gets 3% saline in 100–150 mL boluses, with the 24-hour rise capped at 8–10 mmol/L to avoid osmotic demyelination.
What you must remember
- The five criteria: hypotonic hyponatraemia, inappropriately concentrated urine, urinary sodium over 30 mmol/L, clinical euvolaemia, and exclusion of hypothyroidism, adrenal insufficiency, renal disease and recent diuretics.
- Cheap discriminators: low serum urate and low fractional excretion of urea — both fall in SIADH and both recover with cure; hypouricaemia is a classic MCQ line.
- Cause clusters: malignancy (small cell lung above all, also pancreas, thymus, lymphoma), chest disease (pneumonia, tuberculosis), CNS events (stroke, meningitis, haemorrhage), drugs (carbamazepine and oxcarbazepine, SSRIs, cyclophosphamide, vincristine, cisplatin), and the postoperative state with pain and nausea — the commonest in-hospital trigger.
- Therapy ladder: treat the cause; restrict fluid to 800 mL–1 L daily; add salt tablets with or without a loop diuretic for persistent cases; urea is an option; tolvaptan suits selected chronic cases but risks overcorrection.
- Hypertonic saline discipline: 3% saline 100–150 mL over 10–20 minutes, repeat as needed for seizures or coma, aiming for a 4–6 mmol/L acute lift — enough to clear symptoms, never a full correction.
- The ceiling and its reason: a rise beyond 8–10 mmol/L in 24 hours risks osmotic demyelination syndrome — dysarthria, dysphagia, quadriparesis — with chronic, malnourished, alcoholic and hypokalaemic patients most vulnerable; if overcorrection happens, relower with desmopressin and dextrose.
- Cerebral salt wasting flips management: hypovolaemic and salt-wasting, treated with saline — the fluid restriction that suits SIADH harms it.
The sodium of 118 that needed only eight points
A 66-year-old smoker grows drowsy over four days. Sodium 118 mmol/L, plasma osmolality 242 mOsm/kg, urine osmolality 410 mOsm/kg, urine sodium 68 mmol/L — concentrated and salty urine beside dilute blood. Assessment of volume: euvolaemic. Thyroid function and morning cortisol are normal (the two tests that must precede the label), no diuretics, glucose normal. Chest radiograph shows a right hilar mass; SIADH from small cell lung cancer is the working diagnosis. Because he is encephalopathic, 100 mL of 3% saline runs over 20 minutes, twice, with sodium rechecked after each — it reaches 126, confusion clears, hypertonic saline stops. Maintenance is fluid restriction at 800 mL daily with salt tablets; the sodium settles in the low 130s while the oncology workup proceeds. Two forward-looking points finish the case: chemotherapy may re-trigger hyponatraemia (cyclophosphamide, cisplatin), and incurable disease may need cautious tolvaptan or urea, always within the 8 mmol daily ceiling. The discipline taught here: lift the sodium only as far as symptoms demand, then hand the problem back to the cause.
Where students slip
Speed kills here: correcting 118 to 138 in a day creates the dysarthric, quadriparetic patient a week later — osmotic demyelination follows the cure, and chronic hyponatraemia tolerates rapid correction worst. The second slip is misreading volume: the neurosurgical patient with a normal examination but negative salt balance may have cerebral salt wasting, in which fluid restriction deepens the hyponatraemia; urine sodium is high in both, so volume status and response to saline decide. The third is skipping the exclusions — profound hypothyroidism and glucocorticoid deficiency mimic SIADH biochemistry exactly, and one morning cortisol before the label is the cheapest insurance. Finally, remember postoperative pain and nausea as the stealth cause: the sodium that falls on day three after an uncomplicated operation is more often SIADH than a fluid blunder.
Frequently asked questions
What are the essential diagnostic criteria for SIADH?
Hypotonic hyponatraemia (plasma osmolality under 275 mOsm/kg) with urine osmolality above 100 mOsm/kg, urinary sodium above 30 mmol/L, clinical euvolaemia, and normal thyroid, adrenal and renal function without diuretics.
What is the maximum safe rate of correction?
An increase of 8–10 mmol/L in 24 hours; exceeding it risks osmotic demyelination syndrome, so overcorrection is actively reversed with dextrose water and desmopressin.
What is the immediate treatment of seizing hyponatraemia?
3% saline 100–150 mL over 10–20 minutes, repeated with sodium monitoring, aiming for a 4–6 mmol/L rise to abort seizures.
How is cerebral salt wasting differentiated from SIADH?
Both show concentrated, sodium-rich urine, but cerebral salt wasting is hypovolaemic with negative salt balance and improves with isotonic saline, whereas SIADH is euvolaemic and worsens with it.
What is the role of tolvaptan?
A V2-receptor antagonist for selected chronic SIADH (as in incurable cancer), started in hospital with close sodium monitoring because overcorrection and liver concerns at high doses limit its use.