Euvolemic Hyponatremia with Urine Sodium 80 mmol/L and Urine Osmolality 305 mOsm/kg: SIADH is the Diagnosis
In a euvolemic patient with serum sodium <135 mmol/L, urine sodium 80 mmol/L, and urine osmolality 305 mOsm/kg, the diagnosis is syndrome of inappropriate antidiuretic hormone secretion (SIADH), and first-line management is fluid restriction to 1 L/day. 1, 2
Diagnostic Confirmation
The laboratory findings definitively establish SIADH in this clinical context:
- Urine sodium >20–40 mmol/L (yours is 80 mmol/L) indicates inappropriate renal sodium excretion despite hyponatremia, which is pathognomonic for SIADH in a euvolemic patient 1, 2, 3
- Urine osmolality >100 mOsm/kg (yours is 305 mOsm/kg) demonstrates impaired free water excretion—the kidneys are inappropriately concentrating urine when they should be maximally diluting it 1, 2, 4
- Euvolemic state (no edema, orthostatic hypotension, or volume overload) distinguishes SIADH from hypovolemic causes (urine Na would be <30 mmol/L) and hypervolemic causes (cirrhosis, heart failure) 1, 2
The diagnosis requires exclusion of hypothyroidism and adrenal insufficiency, which can mimic SIADH but require different treatment 2, 5. Check TSH and morning cortisol; if cortisol is low, perform a low-dose ACTH stimulation test 5. Pseudohyponatremia from hyperglycemia or hyperlipidemia must also be ruled out by confirming low serum osmolality 1, 4.
First-Line Management: Fluid Restriction
Fluid restriction to 800–1,200 mL per 24 hours is the cornerstone of SIADH treatment for asymptomatic or mildly symptomatic patients 1, 2, 6, 3. This approach:
- Limits free water intake while the kidneys remain unable to excrete it appropriately 7, 4
- Achieves correction rates averaging 1.0 mEq/L per day, which is safe for chronic hyponatremia 1
- Avoids the risks of hypertonic saline (osmotic demyelination syndrome) in non-emergent cases 1, 6
If fluid restriction alone fails after 48–72 hours, add oral sodium chloride 100 mEq three times daily to increase solute intake and promote water excretion 1, 3.
When to Escalate to Hypertonic Saline
Reserve 3% hypertonic saline for severe symptomatic hyponatremia only—altered mental status, seizures, or coma 1, 2, 6. In these emergencies:
- Administer 100 mL boluses of 3% NaCl IV, repeating up to three times at 10-minute intervals 1
- Target correction of 6 mmol/L over 6 hours or until symptoms resolve 1, 2
- Never exceed 8 mmol/L correction in 24 hours to prevent osmotic demyelination syndrome 1, 2, 6, 4
- Monitor serum sodium every 2 hours during active correction 1
Critical Pitfall: Avoid Normal Saline
Do not use 0.9% normal saline in SIADH—it acts as a hypotonic solution in these patients because the kidneys excrete the sodium while retaining the water, paradoxically worsening hyponatremia 3. Normal saline is appropriate only for hypovolemic hyponatremia (urine Na <30 mmol/L), not SIADH 1, 3.
Identify and Treat the Underlying Cause
SIADH is always secondary to another condition 2, 7. Common causes include:
- Malignancy (especially small cell lung cancer, which produces ectopic ADH) 2, 7
- CNS disorders (meningitis, encephalitis, subarachnoid hemorrhage, traumatic brain injury) 1, 7
- Pulmonary disease (pneumonia, tuberculosis, positive-pressure ventilation) 2, 7
- Medications (SSRIs, carbamazepine, oxcarbazepine, NSAIDs, opioids, cyclophosphamide, vincristine) 1, 2
- Postoperative state (pain, nausea, and stress stimulate nonosmotic ADH release) 7, 3
Discontinue offending medications immediately if identified 1, 2. Treat underlying infections or malignancies; successful cancer treatment often resolves paraneoplastic SIADH 2.
Second-Line Pharmacologic Options
If fluid restriction fails or is poorly tolerated, consider:
- Demeclocycline (induces nephrogenic diabetes insipidus, reducing ADH effect) 1, 2
- Urea (increases solute load, promoting water excretion) 1, 3
- Tolvaptan (vasopressin receptor antagonist, FDA-approved for euvolemic hyponatremia; start 15 mg daily, titrate to 30–60 mg) 1
These agents are reserved for chronic, refractory SIADH because they carry risks of overcorrection and require intensive sodium monitoring 1, 3.
Special Consideration: Cerebral Salt Wasting
In neurosurgical patients (subarachnoid hemorrhage, brain injury), distinguish SIADH from cerebral salt wasting (CSW), which presents identically except for volume status 1, 2. CSW is hypovolemic (orthostatic hypotension, tachycardia, CVP <6 cm H₂O) and requires volume and sodium replacement, not fluid restriction 1. Misdiagnosing CSW as SIADH and applying fluid restriction can precipitate cerebral ischemia and death 1.
Monitoring During Treatment
- Check serum sodium every 24 hours initially, then adjust frequency based on response 1
- Track daily weight and fluid intake/output 1
- Watch for signs of osmotic demyelination syndrome (dysarthria, dysphagia, oculomotor dysfunction, quadriparesis) 2–7 days after correction 1
- If overcorrection occurs (>8 mmol/L in 24 hours), immediately administer D5W or desmopressin to relower sodium 1