What is the treatment approach for hyponatremia?

Treatment of Hyponatremia

The treatment of hyponatremia depends critically on symptom severity, volume status, and rapidity of onset, with the overriding principle being to avoid correction exceeding 8 mmol/L in 24 hours to prevent osmotic demyelination syndrome. 1

Initial Assessment

Before initiating treatment, evaluate the following:

• Serum sodium <131 mmol/L warrants full workup including serum and urine osmolality, urine electrolytes, uric acid, and extracellular fluid (ECF) volume status 2, 1
• Assess volume status by examining for orthostatic hypotension, dry mucous membranes, skin turgor (hypovolemia) versus jugular venous distention, peripheral edema, ascites (hypervolemia) 1
• Determine symptom severity: severe symptoms include seizures, coma, confusion, obtundation, or cardiorespiratory distress; mild symptoms include nausea, vomiting, weakness, headache 1, 3, 4
• Establish chronicity: acute (<48 hours) versus chronic (>48 hours) hyponatremia, as chronic cases require more cautious correction 1, 5

Note: Obtaining ADH and natriuretic peptide levels is not supported by evidence and should not delay treatment 2, 1

Treatment Based on Symptom Severity

Severe Symptomatic Hyponatremia (Medical Emergency)

For patients with seizures, coma, confusion, or cardiorespiratory distress, immediately administer 3% hypertonic saline 1, 3, 4:

• Target correction: 6 mmol/L over 6 hours or until severe symptoms resolve 2, 1
• Administer as 100 mL boluses over 10 minutes, repeatable up to three times at 10-minute intervals 1
• Maximum total correction: 8 mmol/L in 24 hours (not 10-12 mmol/L) to prevent osmotic demyelination syndrome 2, 1, 5
• Monitor serum sodium every 2 hours during initial correction 1
• ICU admission required for close monitoring 1

Mild to Moderate Symptomatic or Asymptomatic Hyponatremia

Treatment is determined by volume status:

Treatment Based on Volume Status

Hypovolemic Hyponatremia

Characterized by: Urine sodium <30 mmol/L, signs of volume depletion (hypotension, tachycardia, dry mucous membranes) 1

Treatment approach:

• Discontinue diuretics immediately 1
• Administer isotonic (0.9%) saline for volume repletion 1, 4
• For severe dehydration with neurological symptoms, consider hypertonic saline with careful monitoring 1
• Correction rate: do not exceed 8 mmol/L in 24 hours 1

Euvolemic Hyponatremia (SIADH)

Characterized by: Euvolemic state, urine sodium >20-40 mmol/L, urine osmolality >300 mOsm/kg, normal thyroid/adrenal function 1

Treatment approach:

• Fluid restriction to 1 L/day is the cornerstone of treatment 2, 1
• If no response to fluid restriction, add oral sodium chloride 100 mEq three times daily 1
• For resistant cases, consider:
  • Urea (40 g in 100-150 mL normal saline every 8 hours) 1
  • Demeclocycline 2, 1
  • Loop diuretics 1
  • Vaptans (tolvaptan 15 mg daily, titrate to 30-60 mg) for persistent cases 1, 6

Important: Vaptans should be used cautiously due to risk of overly rapid correction 1

Hypervolemic Hyponatremia (Heart Failure, Cirrhosis)

Characterized by: Volume overload with edema, ascites, elevated jugular venous pressure 1

Treatment approach:

• Fluid restriction to 1-1.5 L/day for sodium <125 mmol/L 1
• Discontinue diuretics temporarily if sodium <125 mmol/L 1
• For cirrhotic patients, consider albumin infusion alongside fluid restriction 1
• Treat underlying condition (optimize heart failure management, manage cirrhosis) 1, 4
• Avoid hypertonic saline unless life-threatening symptoms present, as it worsens edema and ascites 1
• Vaptans may be considered for persistent severe hyponatremia despite fluid restriction and maximization of guideline-directed therapy 1, 6

Special Populations and Considerations

Neurosurgical Patients

Critical distinction: Cerebral Salt Wasting (CSW) versus SIADH 2, 1:

CSW characteristics:

• Evidence of volume depletion (hypotension, tachycardia, dry mucous membranes) 1
• High urinary sodium (>20 mmol/L) with volume depletion 1
• More common in poor clinical grade, ruptured anterior communicating artery aneurysms, hydrocephalus 1

CSW treatment:

• Volume and sodium replacement with isotonic or hypertonic saline (NOT fluid restriction) 2, 1
• For severe symptoms: 3% hypertonic saline plus fludrocortisone in ICU 2, 1
• Hydrocortisone may prevent natriuresis in subarachnoid hemorrhage patients 1
• Avoid fluid restriction in subarachnoid hemorrhage patients at risk of vasospasm 2, 1

Cirrhotic Patients

Require more cautious correction (4-6 mmol/L per day, maximum 8 mmol/L in 24 hours) due to higher risk of osmotic demyelination syndrome 1, 5:

• Hyponatremia in cirrhosis increases risk of spontaneous bacterial peritonitis (OR 3.40), hepatorenal syndrome (OR 3.45), and hepatic encephalopathy (OR 2.36) 1
• Tolvaptan carries higher risk of gastrointestinal bleeding in cirrhosis (10% vs 2% placebo) 1, 6
• Sodium restriction (not fluid restriction) results in weight loss as fluid follows sodium 1

High-Risk Patients for Osmotic Demyelination Syndrome

Patients with advanced liver disease, alcoholism, malnutrition, severe hyponatremia, hypophosphatemia, hypokalemia, or prior encephalopathy require correction of 4-6 mmol/L per day, not exceeding 8 mmol/L in 24 hours 1, 5

Monitoring During Treatment

• Severe symptoms: monitor serum sodium every 2 hours during initial correction 1
• After resolution of severe symptoms: monitor every 4 hours 1
• Watch for signs of osmotic demyelination syndrome (dysarthria, dysphagia, oculomotor dysfunction, quadriparesis) typically occurring 2-7 days after rapid correction 1, 5

Management of Overcorrection

If sodium correction exceeds 8 mmol/L in 24 hours 1, 5:

• Immediately discontinue current fluids and switch to D5W (5% dextrose in water) 1, 5
• Consider administering desmopressin to slow or reverse the rapid rise 1, 5
• Target: bring total 24-hour correction to no more than 8 mmol/L from starting point 1

Common Pitfalls to Avoid

• Overly rapid correction exceeding 8 mmol/L in 24 hours leading to osmotic demyelination syndrome 1, 5
• Using fluid restriction in cerebral salt wasting, which worsens outcomes 2, 1, 5
• Inadequate monitoring during active correction 1, 5
• Ignoring mild hyponatremia (130-135 mmol/L) as clinically insignificant, when it increases fall risk and mortality 1, 3
• Using hypertonic saline in hypervolemic hyponatremia without life-threatening symptoms 1, 5
• Failing to distinguish between SIADH and CSW in neurosurgical patients 2, 1