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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- SIADH = excess ADH secretion → water retention → dilutional hyponatraemia with euvolaemia
- Diagnostic criteria (Bartter & Schwartz): hyponatraemia (<135), low serum osmolality (<275), inappropriately concentrated urine (osmolality >100), urine Na >30, euvolaemic, no adrenal/thyroid/renal disease
- Common causes: lung disease (pneumonia, SCLC), CNS disease (stroke, SAH, meningitis), drugs (SSRIs, carbamazepine, cyclophosphamide), post-operative pain/nausea
- Diagnosis of EXCLUSION: must exclude hypothyroidism, adrenal insufficiency, diuretics, renal failure
- Treatment: fluid restriction (750–1000 mL/day) first-line. Demeclocycline or tolvaptan (vasopressin receptor antagonist) second-line
- Correct Na⁺ SLOWLY: max 8–10 mmol/L per 24 h. Rapid correction → osmotic demyelination syndrome (central pontine myelinolysis)
Overview
The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is characterised by excess ADH release that is inappropriate for the plasma osmolality or volume status, resulting in impaired water excretion and dilutional hyponatraemia. It is a diagnosis of exclusion — hypothyroidism, adrenal insufficiency, renal impairment, and diuretic use must be ruled out first. Common causes include: pulmonary disease (pneumonia, TB, lung abscess), malignancy (small cell lung cancer is the classic ectopic ADH producer), CNS disorders (stroke, SAH, meningitis, head injury), drugs (SSRIs, carbamazepine, oxcarbazepine, cyclophosphamide, ecstasy), and post-operative pain/nausea. SIADH is one of the most common causes of euvolaemic hyponatraemia in hospitalised patients.
Epidemiology
SIADH is very common in hospitalised patients — it accounts for approximately 30–40% of all hyponatraemia cases. Post-operative SIADH is particularly common (pain, nausea, opioids, and stress all stimulate ADH). Drug-induced SIADH is increasingly recognised, particularly with SSRIs (especially in elderly patients). SCLC-associated SIADH occurs in approximately 10–15% of SCLC cases. Hyponatraemia itself is the most common electrolyte disorder in hospitalised patients, affecting up to 30%.
Clinical Features
Symptoms
Mild hyponatraemia (125–135): often asymptomatic or nonspecific (nausea, malaise, headache)
Moderate (120–125): confusion, lethargy, muscle cramps, unsteadiness
Severe (<120): drowsiness, seizures, coma — medical emergency
Falls (particularly in elderly — even mild hyponatraemia increases fall risk)
Rate of fall matters more than absolute level — acute decline is more dangerous
Signs
Euvolaemic — NO oedema, NO signs of dehydration (this helps differentiate from other causes)
Normal JVP, no peripheral oedema (unlike heart failure/nephrotic cause)
Normal skin turgor, no postural hypotension (unlike hypovolaemic causes)
Seizures and reduced GCS in severe cases
Investigations
First-line
Serum sodium<135 mmol/L (hyponatraemia)
Serum osmolality<275 mOsm/kg (low — confirms dilutional hyponatraemia)
Urine osmolality>100 mOsm/kg (inappropriately concentrated — kidneys retaining water when they should be diluting)
Urine sodium>30 mmol/L (elevated — sodium loss in urine despite low serum sodium)
Second-line
TFTsExclude hypothyroidism (hyponatraemia is associated)
9 AM cortisol / Synacthen testExclude adrenal insufficiency — can cause identical picture to SIADH
Volume status assessmentClinical examination: JVP, skin turgor, BP, oedema — must confirm EUVOLAEMIC
Chest X-rayLook for lung pathology (pneumonia, malignancy)
Specialist
CT chestIf SCLC suspected (smoking history + SIADH)
CT/MRI brainIf CNS cause suspected (stroke, SAH, tumour)
Management
European Society of Endocrinology Clinical Practice Guideline on Hyponatraemia, 2014; NICE CKS1
Treat underlying cause
- Stop offending drugs (SSRIs, carbamazepine, thiazides)
- Treat underlying infection, malignancy, or CNS disease
- Post-operative: usually self-limiting once pain/nausea resolve
2
Fluid restriction (first-line)
- Restrict to 750–1000 mL/day (all oral and IV fluids combined)
- Effective in most cases — expect Na⁺ rise of 1–2 mmol/L per day
- Monitor Na⁺ daily (or more frequently if severe)
3
Second-line therapies
- Demeclocycline 600–1200 mg/day: inhibits ADH action on collecting duct (takes 3–5 days to work). Monitor renal function
- Tolvaptan (vasopressin V2 receptor antagonist): potent aquaresis. Specialist only. Risk of rapid Na⁺ correction — initiate in hospital with close monitoring
- Hypertonic saline (3%): only for SEVERE symptomatic hyponatraemia (seizures, coma) — specialist-led
4
Rate of sodium correction (CRITICAL)
- Maximum rate: 8–10 mmol/L in first 24 hours, 18 mmol/L in first 48 hours
- AVOID rapid correction — risk of osmotic demyelination syndrome (ODS, central pontine myelinolysis)
- ODS: locked-in syndrome, quadriplegia, bulbar palsy — devastating and often irreversible
- If Na⁺ rising too fast: give desmopressin 1–2 mcg IV to slow correction + free water (oral or IV 5% dextrose)
- Monitor Na⁺ every 4–6 hours during active correction
Complications
- Seizures and cerebral oedema: Acute severe hyponatraemia (<120) causes brain cell swelling — medical emergency
- Osmotic demyelination syndrome: From OVERLY RAPID correction of chronic hyponatraemia — pontine and extrapontine demyelination. Devastating, often permanent
- Falls and fractures: Even mild chronic hyponatraemia increases fall risk in elderly (impairs gait and concentration)
- Death: Acute severe hyponatraemia (<120) carries ~10% mortality from cerebral oedema/herniation
UKMLA Exam Tips
- 1SIADH is a diagnosis of EXCLUSION: low serum osmolality + high urine osmolality + euvolaemic + no thyroid/adrenal/renal disease
- 2Classic association: SCLC + hyponatraemia = ectopic ADH production (SIADH)
- 3SSRI-induced hyponatraemia: common exam scenario, especially elderly patient started on sertraline who becomes confused 2 weeks later
- 4Euvolaemic is KEY — if oedema → think heart failure/liver failure/nephrotic syndrome. If dehydrated → think hypovolaemic cause
- 5Rate of correction: MAX 8–10 mmol/L in 24 h. Too fast = osmotic demyelination (central pontine myelinolysis) — permanent quadriplegia
- 6SIADH = opposite of DI. In SIADH: low Na⁺, low serum osm, HIGH urine osm. In DI: high Na⁺, high serum osm, LOW urine osm
- 7Urine Na >30 mmol/L in SIADH (kidneys "wasting" sodium). In hypovolaemic hyponatraemia, urine Na is LOW (<20 — kidneys retaining Na)
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