What is the appropriate management of hyponatremia based on whether it is acute or chronic, the severity of symptoms, and the patient’s volume status?

Hyponatremia Management

Initial Assessment: Determine Acuity and Symptom Severity First

The most critical first step is determining whether hyponatremia is acute (<48 hours) or chronic (>48 hours), and whether the patient has severe symptoms—this distinction fundamentally changes your correction rate and risk of complications. 1

Severe Symptomatic Hyponatremia (Medical Emergency)

Severe symptoms include seizures, coma, altered consciousness, confusion, delirium, or respiratory distress. 1, 2

• Administer 3% hypertonic saline immediately with 100 mL boluses over 10 minutes, repeatable up to three times at 10-minute intervals until symptoms improve. 1, 3
• Target correction of 6 mmol/L over 6 hours or until severe symptoms resolve, but never exceed 8 mmol/L total correction in 24 hours. 1, 3
• Monitor serum sodium every 2 hours during initial correction. 1, 3
• This aggressive approach applies regardless of volume status when life-threatening symptoms are present. 1

Mild to Moderate Symptoms

Symptoms include nausea, vomiting, headache, muscle cramps, gait instability, lethargy, or confusion without severe neurological compromise. 2

• Treatment depends on volume status (see below). 1
• Correction rate should not exceed 8 mmol/L in 24 hours. 1, 3
• Monitor serum sodium every 4-6 hours initially. 1, 3

---

Volume Status Assessment: The Key to Etiology and Treatment

After addressing severe symptoms, assess extracellular fluid volume status through physical examination to determine whether hyponatremia is hypovolemic, euvolemic, or hypervolemic—this guides all subsequent therapy. 1, 3

Hypovolemic Hyponatremia (Volume Depletion)

Clinical signs: Orthostatic hypotension, dry mucous membranes, decreased skin turgor, flat neck veins, tachycardia. 1

Urine sodium <30 mmol/L** suggests extrarenal losses (GI losses, burns, third-spacing); **urine sodium >20 mmol/L suggests renal losses (diuretics, salt-wasting nephropathy). 1

Treatment:

• Discontinue diuretics immediately. 1, 3
• Administer isotonic saline (0.9% NaCl) for volume repletion at 15-20 mL/kg/h initially, then 4-14 mL/kg/h based on response. 1, 3
• Do not exceed 8 mmol/L correction in 24 hours even during volume resuscitation. 1
• Once euvolemic, reassess—if sodium normalizes with volume repletion, continue maintenance fluids; if hyponatremia persists, consider SIADH. 1

Euvolemic Hyponatremia (SIADH)

Clinical signs: No edema, no orthostatic hypotension, normal skin turgor, moist mucous membranes. 1

Diagnostic criteria: Serum osmolality <275 mOsm/kg, urine osmolality >100 mOsm/kg (typically >300 mOsm/kg), urine sodium >20-40 mmol/L, normal thyroid/adrenal/renal function. 1, 3

Treatment:

• Fluid restriction to 1 L/day (or <800 mL/day for refractory cases) is the cornerstone of treatment. 1, 3, 4
• If fluid restriction fails after 48-72 hours, add oral sodium chloride 100 mEq three times daily. 1
• For persistent hyponatremia despite fluid restriction and salt supplementation, consider vasopressin receptor antagonists (tolvaptan 15 mg once daily, titrate to 30-60 mg). 1, 5
• Alternative pharmacologic options include urea, demeclocycline, or lithium, though these have more side effects. 1, 4

Common pitfall: In neurosurgical patients, distinguish SIADH from cerebral salt wasting (CSW)—CSW presents with hypovolemia and requires volume/sodium replacement, NOT fluid restriction. 1

Hypervolemic Hyponatremia (Heart Failure, Cirrhosis)

Clinical signs: Peripheral edema, ascites, jugular venous distention, pulmonary congestion. 1, 3

Treatment:

• Fluid restriction to 1-1.5 L/day for serum sodium <125 mmol/L. 1, 3
• Discontinue diuretics temporarily if sodium <125 mmol/L. 1, 3
• In cirrhotic patients, consider albumin infusion (8 g per liter of ascites removed) alongside fluid restriction. 1, 3
• Avoid hypertonic saline unless life-threatening symptoms are present, as it worsens fluid overload. 1
• Treat underlying condition (optimize heart failure therapy, manage cirrhosis). 3
• For persistent severe hyponatremia despite fluid restriction, consider tolvaptan with extreme caution (higher risk of GI bleeding in cirrhosis: 10% vs 2% placebo). 1, 5

---

Critical Correction Rate Guidelines: Preventing Osmotic Demyelination Syndrome

The single most important safety principle: never exceed 8 mmol/L correction in any 24-hour period. 1, 3, 4

Standard-Risk Patients

• Target 4-8 mmol/L per day, maximum 10-12 mmol/L in 24 hours. 1

High-Risk Patients (Require Slower Correction)

Patients with advanced liver disease, chronic alcoholism, malnutrition, prior encephalopathy, or severe hyponatremia (<120 mmol/L). 1, 3

• Limit correction to 4-6 mmol/L per day, absolute maximum 8 mmol/L in 24 hours. 1, 3
• These patients have a 0.5-1.5% risk of osmotic demyelination syndrome even with careful correction. 1

Management of Overcorrection

If sodium rises >8 mmol/L in 24 hours:

• Immediately discontinue current fluids and switch to D5W (5% dextrose in water). 1, 3
• Consider administering desmopressin to slow or reverse the rapid rise. 1
• Goal: bring total 24-hour correction back to ≤8 mmol/L from baseline. 1

Watch for osmotic demyelination syndrome signs (dysarthria, dysphagia, oculomotor dysfunction, quadriparesis) typically 2-7 days after rapid correction. 1

---

Specific Clinical Scenarios and Pitfalls

Diuretic-Induced Hyponatremia

• For sodium 126-135 mmol/L with normal creatinine: continue diuretics with close monitoring. 3
• For sodium 121-125 mmol/L: consider more cautious approach, may continue with increased monitoring. 3
• For sodium ≤120 mmol/L: stop diuretics immediately and consider volume expansion. 3

Cirrhotic Patients

• Sodium ≤130 mmol/L increases risk of spontaneous bacterial peritonitis (OR 3.40), hepatorenal syndrome (OR 3.45), and hepatic encephalopathy (OR 2.36). 1, 3
• 21.6% of cirrhotic patients have sodium ≤130 mmol/L; only 1.2% have sodium ≤120 mmol/L. 1
• Hyponatremia in cirrhosis is mostly dilutional and hypervolemic. 1

Neurosurgical Patients (Subarachnoid Hemorrhage, Brain Injury)

• Cerebral salt wasting (CSW) is more common than SIADH in this population. 1
• CSW requires volume and sodium replacement with isotonic or hypertonic saline, NEVER fluid restriction. 1
• In subarachnoid hemorrhage patients at risk of vasospasm, fluid restriction is contraindicated. 1
• Consider fludrocortisone 0.1-0.2 mg daily for severe CSW or to prevent vasospasm. 1

Asymptomatic Mild Hyponatremia (130-135 mmol/L)

Do not ignore mild hyponatremia as clinically insignificant. 2

• Even mild chronic hyponatremia increases fall risk (21% vs 5% in normonatremic patients), fractures, cognitive impairment, and mortality (60-fold increase with sodium <130 mmol/L: 11.2% vs 0.19%). 1, 2, 4
• Treatment depends on underlying cause and volume status. 3
• Monitor closely, as progression may require intervention. 2

---

Common Pitfalls to Avoid

1. Correcting chronic hyponatremia faster than 8 mmol/L in 24 hours—this causes osmotic demyelination syndrome. 1, 3
2. Using fluid restriction in cerebral salt wasting—this worsens outcomes and can precipitate cerebral ischemia. 1
3. Inadequate monitoring during active correction—check sodium every 2 hours for severe symptoms, every 4-6 hours for mild symptoms. 1, 3
4. Failing to recognize and treat the underlying cause—hyponatremia is usually a manifestation of another disease process. 1, 6
5. Using hypertonic saline in hypervolemic hyponatremia without life-threatening symptoms—this worsens edema and ascites. 1
6. Ignoring mild hyponatremia (130-135 mmol/L) as clinically insignificant—it carries real morbidity and mortality risk. 2