What is the appropriate treatment approach for hyponatremia?

Treatment of Hyponatremia

The treatment of hyponatremia depends critically on symptom severity, volume status, and chronicity—with severe symptomatic hyponatremia requiring immediate 3% hypertonic saline to prevent cerebral herniation, while chronic asymptomatic cases are managed according to volume status (isotonic saline for hypovolemia, fluid restriction for euvolemia/SIADH, and fluid restriction plus treatment of underlying disease for hypervolemia). 1

Immediate Management Based on Symptom Severity

Severe Symptomatic Hyponatremia (Medical Emergency)

For patients with severe symptoms—seizures, coma, altered consciousness, confusion, or respiratory distress—administer 100 mL of 3% hypertonic saline intravenously over 10 minutes immediately. 1, 2 This can be repeated every 10 minutes up to three total boluses if symptoms persist. 1, 2

• Target correction: Increase serum sodium by 4-6 mEq/L within the first 1-2 hours or until severe symptoms resolve. 1, 3, 4
• Absolute safety limit: Never exceed 8 mmol/L correction in any 24-hour period to prevent osmotic demyelination syndrome. 1, 2, 3
• Monitoring: Check serum sodium every 2 hours during initial correction phase. 1, 2

Mild to Moderate Symptomatic Hyponatremia

For patients with nausea, vomiting, headache, weakness, or mild confusion but without severe neurological symptoms, treatment is guided by volume status and underlying cause rather than immediate hypertonic saline. 5, 6

Treatment Algorithm Based on Volume Status

Hypovolemic Hyponatremia

Discontinue diuretics immediately and administer isotonic saline (0.9% NaCl) for volume repletion. 1, 6

• Initial infusion rate: 15-20 mL/kg/hour for the first hour, then 4-14 mL/kg/hour based on response. 1
• Diagnostic clue: Urine sodium <30 mmol/L predicts good response to saline (positive predictive value 71-100%). 1
• Correction rate: Standard patients 4-8 mEq/L per day; high-risk patients (cirrhosis, alcoholism, malnutrition) 4-6 mEq/L per day maximum. 1

Euvolemic Hyponatremia (SIADH)

Fluid restriction to 1 liter per day is the cornerstone of treatment for SIADH. 1, 6, 7

• If fluid restriction fails: Add oral sodium chloride 100 mEq three times daily. 1
• Second-line pharmacologic options: Urea, vasopressin receptor antagonists (tolvaptan 15 mg daily, titrate to 30-60 mg), demeclocycline, or lithium. 1, 8, 3
• For severe symptoms: Use 3% hypertonic saline as described above, then transition to fluid restriction once symptoms resolve. 1

Hypervolemic Hyponatremia (Heart Failure, Cirrhosis)

Implement fluid restriction to 1-1.5 L/day for serum sodium <125 mmol/L. 1, 6

• Discontinue diuretics temporarily if sodium <125 mmol/L. 1
• For cirrhotic patients: Consider albumin infusion (8 g per liter of ascites removed) alongside fluid restriction. 1
• Avoid hypertonic saline unless life-threatening symptoms are present, as it worsens ascites and edema. 1
• Vaptans may be considered for persistent severe hyponatremia despite fluid restriction and optimization of guideline-directed therapy, but use with extreme caution in cirrhosis due to hepatotoxicity risk and increased gastrointestinal bleeding (10% vs 2% placebo). 1

Critical Safety Considerations: Preventing Osmotic Demyelination Syndrome

The single most important principle is never exceeding 8 mmol/L sodium correction in 24 hours. 1, 2, 3

High-Risk Populations Requiring Slower Correction (4-6 mEq/L per day maximum)

• Advanced liver disease or cirrhosis 1
• Chronic alcoholism 1, 3
• Malnutrition 1
• Prior hepatic encephalopathy 1
• Severe hyponatremia (<120 mmol/L) of chronic duration 1

These patients have a 0.5-1.5% risk of osmotic demyelination syndrome even with careful correction. 1

Managing Overcorrection

If sodium rises too rapidly (>8 mmol/L in 24 hours):

• Immediately discontinue current fluids and switch to D5W (5% dextrose in water). 1
• Administer desmopressin to slow or reverse the rapid rise. 1
• Target: Bring total 24-hour correction back to ≤8 mmol/L from baseline. 1

Special Populations and Contexts

Neurosurgical Patients: Distinguishing SIADH from Cerebral Salt Wasting

In patients with subarachnoid hemorrhage, brain injury, or neurosurgical conditions, distinguishing cerebral salt wasting (CSW) from SIADH is critical because they require opposite treatments. 1, 2

SIADH characteristics:

• Euvolemic (normal volume status) 1
• Urine sodium >20-40 mEq/L 1
• Urine osmolality >300 mOsm/kg 1
• Treatment: Fluid restriction to 1 L/day 1

Cerebral Salt Wasting characteristics:

• Hypovolemic (orthostatic hypotension, dry mucous membranes, tachycardia, CVP <6 cm H₂O) 1
• Urine sodium >20 mEq/L despite volume depletion 1
• Treatment: Volume and sodium replacement with isotonic or hypertonic saline (50-100 mL/kg/day) 1
• For severe symptoms: 3% hypertonic saline plus fludrocortisone 0.1-0.2 mg daily 1

Critical pitfall: Using fluid restriction in cerebral salt wasting worsens outcomes and can precipitate cerebral ischemia. 1, 2

In subarachnoid hemorrhage patients at risk of vasospasm, never use fluid restriction—treat presumptively as CSW with volume expansion. 1

Cirrhotic Patients

Hyponatremia in cirrhosis (serum sodium <130 mmol/L) significantly increases risk of complications:

• Spontaneous bacterial peritonitis (OR 3.40) 1
• Hepatorenal syndrome (OR 3.45) 1
• Hepatic encephalopathy (OR 2.36) 1

Management approach:

• Fluid restriction to 1-1.5 L/day for sodium <125 mmol/L 1
• Albumin infusion 1
• Correction rate: Maximum 4-6 mEq/L per day, never exceeding 8 mEq/L in 24 hours 1
• Note: Fluid restriction may prevent further decline but rarely improves sodium significantly—it is sodium restriction (not fluid restriction) that results in weight loss as fluid follows sodium. 1

Acute vs. Chronic Hyponatremia

Acute hyponatremia (<48 hours duration) causes more severe symptoms at the same sodium level and can be corrected more rapidly without risk of osmotic demyelination. 1, 5

Chronic hyponatremia (>48 hours) requires slower, more cautious correction due to brain adaptation. 1

Monitoring Protocol

During Active Correction

• Severe symptoms: Check serum sodium every 2 hours initially 1, 2
• After symptom resolution: Check every 4-6 hours 1
• Mild symptoms or asymptomatic: Check every 24 hours initially 1
• Monitor for osmotic demyelination syndrome signs: Dysarthria, dysphagia, oculomotor dysfunction, quadriparesis (typically 2-7 days after rapid correction) 1

Ongoing Management

• Track daily weights and strict intake/output 2
• Monitor concurrent electrolytes (potassium, magnesium) and correct aggressively 1
• Reassess volume status regularly 1

Common Pitfalls to Avoid

• Ignoring mild hyponatremia (130-135 mmol/L) as clinically insignificant—even mild chronic hyponatremia increases fall risk (21% vs 5%), mortality (60-fold increase for sodium <130 mmol/L), and cognitive impairment. 1, 5, 3
• Correcting chronic hyponatremia faster than 8 mmol/L in 24 hours—this causes osmotic demyelination syndrome. 1, 2
• Using fluid restriction in cerebral salt wasting—this worsens hypovolemia and outcomes. 1, 2
• Failing to recognize and treat the underlying cause—hyponatremia will recur. 1
• Using hypertonic saline in hypervolemic hyponatremia without life-threatening symptoms—this worsens edema and ascites. 1
• Inadequate monitoring during active correction—sodium can rise unpredictably. 1
• Relying on physical examination alone for volume assessment—sensitivity is only 41%, specificity 80%. 1

Clinical Significance of Hyponatremia

Even mild chronic hyponatremia is associated with significant morbidity beyond acute symptoms:

• Cognitive impairment and altered memory 5, 3
• Increased fall risk and fractures 5, 3
• Gait instability and balance disturbances 5
• Increased hospital mortality 5
• Correction of hyponatremia significantly improves cognitive function and quality of life. 5