Quick Reference
Overview and Recommendations
Background
- •Define SIADH as a state of caused by non-osmotic AVP secretion.
- •Identify common triggers including , traumatic brain injury, stroke, and pneumonia.
- •Review medication history for offending agents such as , carbamazepine, cyclophosphamide, and NSAIDs.
- •Recognize that the pathophysiology involves constitutive activation of channels in the renal collecting ducts.
- •Distinguish from (CSWS), which presents with hypovolemia and high urine output.
Evaluation
- •Confirm hypotonic hyponatremia with serum sodium <135 mEq/L and serum osmolality <275 mOsm/kg.
- •Document inappropriate urine concentration with urine osmolality >100 mOsm/kg.
- •Obtain spot urine sodium; levels >30 mmol/L suggest SIADH in the setting of normal salt intake.
- •Rule out and by checking TSH and morning cortisol levels.
- •Assess clinical volume status to ensure the patient is euvolemic (absence of edema, ascites, or orthostatic hypotension).
- •Calculate fractional excretion of uric acid (FEUrate); a value >12% strongly supports SIADH.
- •Order chest X-ray or CT to screen for occult pulmonary malignancy or infection.
Management
- •Administer Hypertonic Saline (3% NaCl) 100–150 mL IV bolus over 20 minutes for severe symptoms (seizures, coma).
- •Limit sodium correction to <10 mmol/L in the first 24 hours to avoid .
- •Initiate fluid restriction to 800–1000 mL/day as first-line therapy for asymptomatic or mild cases.
- •Consider Tolvaptan 7.5 mg to 15 mg orally once daily for patients refractory to fluid restriction.
- •Administer oral urea 15–30 g daily to induce osmotic diuresis in chronic or oncology-related cases.
- •Utilize loop diuretics (e.g., Furosemide 20 mg) combined with salt tablets to increase solute-free water clearance.
- •Discontinue any suspected offending medications immediately.
- •Monitor serum sodium every 4–6 hours during the active correction phase.
Board Review — High Yield
- •Small Cell Lung Cancer — The classic paraneoplastic cause of ectopic ADH production.
- •Euvolemia — The essential clinical volume status required for SIADH diagnosis.
- •Osmotic Demyelination Syndrome — The catastrophic neurological consequence of correcting sodium too rapidly, often affecting the pons.
- •Urine Osmolality >100 mOsm/kg — The hallmark of 'inappropriate' concentration in the face of serum hypotonicity.
- •Hypouricemia — Low serum uric acid (<4 mg/dL) is common due to increased urate clearance.
- •V2 Receptor — The specific vasopressin receptor in the kidney targeted by AVP and antagonized by vaptans.
- •Copeptin — A stable surrogate biomarker for AVP that is elevated in SIADH.
- •Reset Osmostat — A variant of SIADH where ADH is regulated but at a lower osmotic threshold.
Deep Dive — Evidence Details
References
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