How should I evaluate and manage hyponatremia, considering whether it is acute or chronic, the severity of serum sodium reduction, presence of symptoms, and the patient's volume status?

Evaluation and Management of Hyponatremia

Initial Diagnostic Workup

Begin by confirming true hypotonic hyponatremia through serum osmolality measurement (normal 275-290 mOsm/kg), as pseudohyponatremia from hyperglycemia or hyperlipidemia must be excluded first. 1

Once hypotonic hyponatremia is confirmed, obtain:

• Urine osmolality and urine sodium concentration to assess water excretion capacity and differentiate causes 1
• Serum creatinine, BUN, glucose, and electrolytes (potassium, calcium, magnesium) to evaluate renal function and exclude other metabolic derangements 1
• Thyroid-stimulating hormone (TSH) to rule out hypothyroidism 1
• Assessment of extracellular fluid volume status through physical examination, looking specifically for orthostatic hypotension, dry mucous membranes, decreased skin turgor (hypovolemia), or peripheral edema, ascites, and jugular venous distention (hypervolemia) 1

Serum uric acid <4 mg/dL has a 73-100% positive predictive value for SIADH, though this may include cerebral salt wasting in neurosurgical patients. 1

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Determine Acuity and Symptom Severity

Acute vs. Chronic Hyponatremia

The single most critical distinction is whether hyponatremia developed in <48 hours (acute) versus >48 hours (chronic), as this fundamentally determines safe correction rates. 1, 2

• Acute hyponatremia (<48 hours) causes more severe symptoms at the same sodium level and can be corrected more rapidly without risk of osmotic demyelination 2
• Chronic hyponatremia (>48 hours) requires slower, more cautious correction with a maximum of 8 mmol/L in 24 hours 1

Symptom Classification

Severe symptoms (medical emergency): confusion, delirium, altered consciousness, seizures, coma, respiratory distress 2, 3

Mild-to-moderate symptoms: nausea, vomiting, headache, muscle cramps, gait instability, lethargy, weakness, dizziness 2, 3

Asymptomatic or minimally symptomatic: no overt neurological manifestations but may have subtle cognitive impairment 2

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Treatment Based on Symptom Severity

Severe Symptomatic Hyponatremia (Seizures, Coma, Altered Mental Status)

Administer 3% hypertonic saline immediately with an initial goal to correct 6 mmol/L over 6 hours or until severe symptoms resolve. 1, 4

• Give 100 mL boluses of 3% NaCl over 10 minutes, repeating up to three times at 10-minute intervals until symptoms improve 1
• Total correction must not exceed 8 mmol/L in any 24-hour period to prevent osmotic demyelination syndrome 1, 4
• Monitor serum sodium every 2 hours during initial correction 1, 4
• Admit to ICU for close monitoring during active correction 1

Once severe symptoms resolve, discontinue 3% saline and transition to protocols for mild symptoms or asymptomatic hyponatremia. 4

• Switch to monitoring sodium every 4 hours instead of every 2 hours 4
• If initial 6 mmol/L correction achieved in 6 hours, only 2 mmol/L additional correction is allowed in the next 18 hours 4

Mild-to-Moderate Symptomatic or Asymptomatic Hyponatremia

Treatment depends on volume status assessment—this is the decisive factor guiding opposite therapeutic strategies. 1

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Treatment Based on Volume Status

Hypovolemic Hyponatremia

Characterized by: orthostatic hypotension, dry mucous membranes, decreased skin turgor, flat neck veins, urine sodium typically <30 mmol/L 1

Treatment:

• Discontinue diuretics immediately if sodium <125 mmol/L 1
• 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
• Urinary sodium <30 mmol/L has a 71-100% positive predictive value for response to saline infusion 1
• Avoid hypotonic fluids (0.45% saline, lactated Ringer's, D5W) as they worsen hyponatremia 1

Euvolemic Hyponatremia (SIADH)

Characterized by: normal volume status (no edema, no orthostatic hypotension, normal skin turgor, moist mucous membranes), urine sodium >20-40 mmol/L, urine osmolality >300 mOsm/kg 1

Treatment:

• Fluid restriction to 1 L/day is the cornerstone of treatment 1, 5
• If no response to fluid restriction, add oral sodium chloride 100 mEq three times daily 1
• For resistant cases, consider vasopressin receptor antagonists (tolvaptan 15 mg once daily, titrate to 30-60 mg) or urea 1, 5
• Demeclocycline, lithium, or loop diuretics are alternative pharmacological options 1

Hypervolemic Hyponatremia (Heart Failure, Cirrhosis)

Characterized by: peripheral edema, ascites, jugular venous distention, pulmonary congestion 1

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
• For cirrhotic patients, consider albumin infusion (6-8 g per liter of ascites drained) alongside fluid restriction 1
• Avoid hypertonic saline unless life-threatening symptoms are present, as it worsens ascites and edema 1
• Vasopressin receptor antagonists (tolvaptan) may be considered for persistent severe hyponatremia despite fluid restriction, but use with extreme caution in cirrhosis due to higher risk of gastrointestinal bleeding (10% vs. 2% placebo) 1

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Critical Correction Rate Guidelines

The maximum correction of serum sodium is 8 mmol/L in any 24-hour period for standard-risk patients. 1, 6

For high-risk patients (advanced liver disease, alcoholism, malnutrition, prior encephalopathy), limit correction to 4-6 mmol/L per day, maximum 8 mmol/L in 24 hours. 1, 6

Calculate sodium deficit using: Desired increase in Na (mEq/L) × (0.5 × ideal body weight in kg) 1

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Special Considerations in Neurosurgical Patients

In patients with CNS pathology, distinguishing SIADH from cerebral salt wasting (CSW) is critical because they require opposite treatments. 1

Cerebral Salt Wasting (CSW)

Characterized by: true hypovolemia with CVP <6 cm H₂O, urine sodium >20 mmol/L despite volume depletion, clinical signs of hypovolemia (orthostatic hypotension, tachycardia, dry mucous membranes) 1

Treatment:

• Volume and sodium replacement with isotonic or hypertonic saline (50-100 mL/kg/day), NOT fluid restriction 1
• Fludrocortisone 0.1-0.2 mg daily for severe symptoms 1
• Hydrocortisone may prevent natriuresis in subarachnoid hemorrhage patients 1
• Fluid restriction in CSW worsens outcomes and can precipitate cerebral ischemia 1

In subarachnoid hemorrhage patients at risk of vasospasm, hyponatremia should never be treated with fluid restriction. 1

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Management of Overcorrection

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

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

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

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Common Pitfalls to Avoid

• Overly rapid correction of chronic hyponatremia exceeding 8 mmol/L in 24 hours causes osmotic demyelination syndrome 1, 6
• Inadequate monitoring during active correction leads to overcorrection 1
• Using fluid restriction in cerebral salt wasting worsens outcomes 1
• Failing to recognize and treat the underlying cause perpetuates hyponatremia 1
• Using hypertonic saline in hypervolemic hyponatremia without life-threatening symptoms worsens fluid overload 1
• Ignoring mild hyponatremia (130-135 mmol/L) as clinically insignificant—even mild chronic hyponatremia increases fall risk (21% vs. 5%), mortality (60-fold increase with sodium <130 mmol/L), and cognitive impairment 1, 2
• Misdiagnosing CSW as SIADH in neurosurgical patients leads to inappropriate fluid restriction and potential cerebral ischemia 1

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Monitoring Protocol

For severe symptoms: Monitor serum sodium every 2 hours during initial correction 1, 4

After resolution of severe symptoms: Monitor every 4 hours 1, 4

For mild symptoms or asymptomatic patients: Monitor every 24-48 hours initially 1

Continue treatment until sodium reaches 125-130 mmol/L (not normal range), as this is the therapeutic goal for acute correction 1, 6