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Internal Medicine›Condition·Updated Apr 16, 2026·v1

SIADH

SIADH is a common cause of euvolemic hyponatremia characterized by inappropriate AVP activity. Diagnosis requires excluding other causes of hypotonicity and confirming concentrated urine. Treatment ranges from fluid restriction to hypertonic saline, with a strict focus on avoiding rapid overcorrection.

High Evidence198 references·7,600 words·31 min read·v1
hyponatremiaendocrinologynephrologyparaneoplasticinternal medicine

Quick Reference

RxDrug of choiceFluid restriction (non-pharmacological); Tolvaptan 7.5-15 mg PO daily (pharmacological)
AltAlternativesOral Urea (30 g/day), Loop diuretics (Furosemide 20-40 mg) plus Salt tablets
⊘Avoid0.9% Normal Saline (may worsen hyponatremia); Tolvaptan in patients with liver disease
DxTest of choiceSerum and Urine Osmolality + Urine Sodium
ScKey scoreSchwartz and Bartter Criteria
→When to referSevere symptomatic hyponatremia (Na <120 mmol/L), failure of fluid restriction, or suspected paraneoplastic origin
SIADH is a diagnosis of exclusion presenting as euvolemic hyponatremia with concentrated urine; management centers on water restriction and cautious sodium correction.
The Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH) is the most prevalent cause of euvolemic [[hyponatremia]] in hospitalized patients. It is characterized by the non-physiological release of [[arginine vasopressin]] (AVP) or increased renal sensitivity to it, leading to impaired free-water excretion and dilutional hyponatremia. The diagnosis is primarily biochemical, requiring the presence of hypotonic hyponatremia, inappropriately concentrated urine, and clinical euvolemia, while excluding renal, adrenal, and thyroid dysfunction. Common etiologies include malignancies (classically [[Small Cell Lung Cancer]]), central nervous system disorders, pulmonary infections, and various medications such as [[Selective serotonin reuptake inhibitors]] (SSRIs). Management focuses on treating the underlying cause, fluid restriction, and, in severe cases, cautious correction with hypertonic saline to avoid the devastating complication of [[osmotic demyelination syndrome]].

Overview and Recommendations

Background

  • •Identify SIADH as the leading cause of euvolemic , often triggered by ectopic AVP production or enhanced hypothalamic release.
  • •Recognize (SCLC) as the most common paraneoplastic association, occurring in up to 15-45% of cases.
  • •Screen for neurological triggers including , , and post-pituitary surgery.
  • •Review medication history for common culprits: (SSRIs), , , and .
  • •Distinguish from (CSW), which presents with similar biochemistry but involves true volume depletion (hypovolemia).

Evaluation

  • •Confirm hypotonic hyponatremia: Serum sodium <135 mmol/L and serum osmolality <275 mOsm/kg.
  • •Obtain urine osmolality: A value >100 mOsm/kg indicates inappropriately concentrated urine in the setting of serum hypotonicity.
  • •Measure urinary sodium: Concentration >30-40 mmol/L is typical during normal salt and water intake.
  • •Assess volume status: Confirm clinical by the absence of edema, ascites, or signs of dehydration (e.g., orthostasis).
  • •Rule out mimics: Obtain TSH and morning cortisol to exclude and .
  • •Calculate Fractional Excretion of Uric Acid (FEurate): A value >12% supports SIADH; normalization after sodium correction confirms the diagnosis.
  • •Utilize as a surrogate marker for AVP if the diagnosis remains ambiguous.

Management

  • •Administer Hypertonic Saline (3% NaCl) 100-150 mL IV bolus over 10-20 minutes for severe symptoms (seizures, coma, or severe confusion).
  • •Limit correction rate: Avoid increasing serum sodium by >8-10 mmol/L in 24 hours to prevent (ODS).
  • •Implement Fluid Restriction <800-1000 mL/day as the first-line intervention for asymptomatic or mildly symptomatic patients.
  • •Consider 7.5-15 mg PO daily for patients failing fluid restriction; monitor sodium closely every 6-8 hours during initiation.
  • •Prescribe oral Urea 15-30 g/day to induce osmotic diuresis in chronic or refractory cases.
  • •Avoid 0.9% Normal Saline: This may paradoxically worsen hyponatremia via the 'desalination' phenomenon if urine osmolality is high.
  • •Treat the underlying cause: Discontinue offending medications or initiate therapy for the primary malignancy or infection.

Board Review — High Yield

  • •Small Cell Lung Cancer — The classic paraneoplastic cause of SIADH due to ectopic AVP production.
  • •Euvolemia — The hallmark physical exam finding; patients lack both edema and signs of dehydration.
  • •Urine Osmolality >100 mOsm/kg — Inappropriately high concentration despite low serum osmolality (<275 mOsm/kg).
  • •Osmotic Demyelination Syndrome — A permanent neurological injury caused by correcting chronic hyponatremia too rapidly.
  • •Desalination — Paradoxical worsening of hyponatremia after giving isotonic saline because the kidney excretes the salt but keeps the water.
  • •Fractional Excretion of Uric Acid >12% — A high FEurate in a hyponatremic patient is highly suggestive of SIADH.
  • •SSRIs — The most common class of medications associated with drug-induced SIADH, especially in the elderly.
  • •V2 Receptor Antagonists — The mechanism of action for 'vaptans' like Tolvaptan, which block AVP-mediated water reabsorption.

Deep Dive — Evidence Details

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