Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

Volume status is the entire diagnosis - SIADH and cerebral salt wasting produce a nearly identical lab picture: hyponatremia, urine sodium above 40 mEq/L, urine osmolality above 100 mOsm/kg, no edema. Volume is the discriminator. SIADH patients are euvolemic to hypervolemic — normal blood pressure, moist mucous membranes, normal skin turgor, no JVD. Cerebral salt wasting patients are hypovolemic — hypotension, low central venous pressure, poor turgor, elevated hematocrit. Settle this before you write a fluid order.

The treatments are opposite, so getting it wrong hurts - SIADH is fluid restriction, targeting under 800 mL/day, with salt tablets or intravenous saline if it persists and furosemide added when urine osmolality is much higher than serum. Cerebral salt wasting is isotonic saline and sodium repletion. Fluid-restricting a salt-waster deepens the hypovolemia; volume-loading SIADH makes the hyponatremia worse.

Isotonic saline can lower the sodium further - In SIADH urine osmolality often runs above 500 mOsm/kg, roughly twice the serum. Any fluid whose osmolality is below the urine's gets its water retained and its solute excreted, so normal saline can drive the sodium down. Correcting requires a fluid more concentrated than the urine, which is what 3% saline at 513 mOsm/kg is for.

Rule out the mimics before you commit - Hypothyroidism and adrenal insufficiency both produce a SIADH picture and are corrected by hormone replacement, so check thyroid function and cortisol first. Renal function tests and a glucose sort out uremia and pseudohyponatremia. A useful tiebreaker: in SIADH the BUN, creatinine, and serum uric acid run normal or low.

Correction rate is what kills - The ceiling is 8 mEq/L in 24 hours, or 0.5 to 1 mEq/L per hour. Faster than that causes osmotic demyelination of the CNS and a locked-in patient. Work from the hyponatremia entry for the full correction algorithm rather than eyeballing a drip rate.

The symptomatic patient gets salt, not restriction - Seizures, confusion, or delirium need urgent hypertonic saline over the first few hours, not water restriction. A 100 mL bolus of 3% saline is given over the first 3 to 4 hours with a sodium redrawn at 2 to 3 hours to titrate the next dose; a 3 to 4 mEq/L rise in those first hours is justified when the patient is seizing. Repeat boluses if mental status has not improved.

Read the sodium alongside how fast it got there - Nausea and malaise start around 125 to 130 mEq/L, and vomiting in acute hyponatremia is an ominous sign. Headache, lethargy, and obtundation follow, with coma and respiratory arrest below 115 to 120 mEq/L. A chronically hyponatremic patient at 120 may be entirely asymptomatic because the brain has adapted — the same number arrived at overnight is an emergency. Premenopausal women are the group in which acute hyponatremic encephalopathy is most likely to leave permanent damage.

Anesthesia and surgery make it worse - ADH release driven by pain afferents is part of the normal surgical response, and postoperative SIADH is common in hospitalized patients given hypotonic fluids on top of it. Do not run hypotonic maintenance fluid in a patient who is already hyponatremic, and treat pain well, since the afferent traffic is part of the stimulus.

Read the medication list carefully - Carbamazepine and oxcarbazepine increase sensitivity to ADH, chlorpropamide increases V2 receptor number, and SSRIs (especially over 65) and cyclophosphamide are frequent offenders — high-dose IV cyclophosphamide given with a fluid load to prevent hemorrhagic cystitis is a particular trap. Drug-induced SIADH resolves promptly once the agent is stopped. Watch what you give as well: vasopressin, desmopressin, and oxytocin all act at V2 receptors and will do the same thing.

Hunt for the source - Small cell lung cancer is the most common tumor producing ectopic ADH, so a smoker with weight loss or pulmonary symptoms needs a chest x-ray and CT. Any CNS abnormality — stroke, hemorrhage, infection, trauma — can drive it, as can pneumonia of any cause and HIV infection.

Vaptans for the refractory case - Conivaptan intravenously and tolvaptan orally antagonize V2 receptors and are approved for severe persistent SIADH; IV conivaptan is effective at restoring both the sodium and baseline mental status in hospitalized patients. Tolvaptan is hepatotoxic and is off the table in liver disease. Demeclocycline and lithium work but are nephrotoxic and belong last.

Slow to wake, check a sodium - Cerebral edema from a falling sodium presents as lethargy and obtundation and will not respond to naloxone or flumazenil. In a patient at risk, send a sodium before you assume residual anesthetic.

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is unsuppressed release of antidiuretic hormone (ADH) — from the pituitary, from an ectopic source, or continued action at vasopressin-2 receptors — despite a plasma osmolality low enough that it should have shut off. ADH opens aquaporin-2 channels in the cortical and medullary collecting tubules, so free water is reabsorbed and the patient becomes hyponatremic while staying euvolemic to mildly hypervolemic. The normal osmotic threshold for ADH release is roughly 280 to 290 mOsm/kg; in SIADH the hormone keeps working below it.

The perioperative relevance is that surgery itself is a cause — ADH hypersecretion mediated by pain afferents — layered on top of pneumonia, CNS insults, small cell lung cancer, and a long drug list. The harm comes from water moving into brain cells as the sodium falls, producing cerebral edema; how fast it fell matters far more than the absolute number.