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RN Nursing · Endocrine Disorders

SIADH (Syndrome of Inappropriate Antidiuretic Hormone): Nursing Study Guide

By Nurse Jude · Updated June 19, 2026

A focused review of SIADH covering pathophysiology, causes, lab findings, symptoms, treatment, and nursing priorities, with a comparison to diabetes insipidus.

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SIADH is a high-yield endocrine disorder where excess antidiuretic hormone causes water retention and dilutional hyponatremia. Understanding the fluid-and-sodium relationship — and how it differs from diabetes insipidus — is essential for safe nursing care and exam success.

What Is SIADH?

  • SIADH occurs when the body releases too much antidiuretic hormone (ADH).
  • Excess ADH causes the kidneys to retain excessive water.
  • Retained water dilutes sodium in the blood, causing hyponatremia.
  • Key concept: the problem is too much water, not too little sodium.

Pathophysiology

  • ADH is normally released when the body is dehydrated or blood pressure drops.
  • In SIADH, ADH is released even when the body does not need more water.
  • Excess water is retained, blood volume expands, and sodium becomes diluted.
  • Result: hyponatremia with serum sodium below 135 mEq/L.
  • Low sodium causes brain cells to swell.
  • Patients do not appear edematous because fluid distributes into cells, not interstitial tissues.

Memory trick: SIADH = the body is drowning in its own water.

Causes and Triggers

Category Causes
CNS disorders Head injury, stroke, meningitis, brain tumors
Pulmonary conditions Small cell lung cancer (most common exam cause), pneumonia, TB, mechanical ventilation
Medications SSRIs, carbamazepine, cyclophosphamide, NSAIDs, thiazide diuretics
Other Major surgery, pain, stress

Small cell lung cancer is the most commonly tested cause of SIADH because it produces ectopic ADH.

Signs and Symptoms

Symptoms progress as serum sodium falls:

  • Mild hyponatremia (Na⁺ 125–134 mEq/L): nausea, vomiting, headache, fatigue, muscle cramps.
  • Moderate hyponatremia (Na⁺ 115–124 mEq/L): confusion, lethargy, decreased reflexes, personality changes.
  • Severe hyponatremia (Na⁺ <115 mEq/L): seizures, coma, death.

Key Physical Findings

  • Concentrated urine despite normal or high fluid intake.
  • No edema and no signs of dehydration.
  • Weight gain from fluid retention without visible puffiness.

Exam trap: Patients with SIADH are fluid overloaded but do not look edematous.

Key Lab Values

Lab SIADH Finding Why
Serum sodium <135 mEq/L Diluted by retained water
Serum osmolality <280 mOsm/kg Blood is diluted
Urine sodium >20 mEq/L Kidneys still spilling sodium
Urine osmolality >100 mOsm/kg Urine inappropriately concentrated
BUN and creatinine Low or normal Diluted by fluid overload

Memory trick: In SIADH, everything in the blood is low and everything in the urine is high.

SIADH vs. Diabetes Insipidus

Feature SIADH Diabetes Insipidus
ADH level Too high Too low
Water retained Yes No (water is lost)
Serum sodium Low High
Urine output Low and concentrated High and dilute
Serum osmolality Low High
Treatment Fluid restriction Fluid replacement, vasopressin

Treatment

Fluid Restriction

  • Cornerstone of SIADH treatment.
  • Restrict fluids to 800–1000 mL/day.
  • Allows the body to slowly correct sodium naturally.

Hypertonic Saline (3% NaCl)

  • Reserved for severe symptomatic hyponatremia (seizures, altered mental status).
  • Must be given slowly — rapid correction can cause osmotic demyelination syndrome.

Osmotic Demyelination Syndrome

  • Devastating neurological complication from correcting sodium too rapidly.
  • The brain adapts to chronic low sodium and cannot tolerate sudden changes.
  • Do not correct sodium faster than 8–10 mEq/L in 24 hours.

Medications for Chronic SIADH

  • Demeclocycline — blocks ADH action at the kidney tubules.
  • Tolvaptan and conivaptan — vasopressin receptor antagonists that promote free water excretion.

Treat the Underlying Cause

  • Remove a tumor, treat pneumonia, or stop the offending medication.
  • Resolving the cause often resolves SIADH entirely.

Nursing Priorities

  • Implement strict fluid restriction and teach the patient why it matters.
  • Monitor serum sodium frequently for worsening or overcorrection.
  • Assess neurological status continuously for confusion, seizures, or declining consciousness.
  • When giving hypertonic saline, administer via IV pump slowly and check sodium every 2 hours.
  • Monitor intake and output strictly; weigh the patient daily.
  • Implement seizure precautions for any patient with sodium <120 mEq/L.

Patient Teaching

  • Follow fluid restriction even when thirsty.
  • Know warning signs of worsening hyponatremia: headache, confusion, seizures.
  • Seek emergency care immediately if these symptoms occur.
  • Avoid excess free water — plain water, ice chips, and water-rich foods.
  • If SIADH is caused by a medication, do not stop it without consulting the provider.

Key Takeaways

  • SIADH = excess ADH → water retention → dilutional hyponatremia.
  • Classic NCLEX cause is small cell lung cancer producing ectopic ADH.
  • Patients are fluid overloaded but have no visible edema.
  • Labs: serum sodium and osmolality low; urine sodium and osmolality high.
  • First-line treatment is fluid restriction; hypertonic saline is reserved for severe symptoms.
  • Never correct sodium faster than 8–10 mEq/L per 24 hours to prevent osmotic demyelination syndrome.

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