How should I assess and manage hyponatremia, including determining acute versus chronic onset, severity, symptoms, and appropriate treatment based on volume status (hypovolemic, euvolemic, hypervolemic) and possible medication‑induced causes?

Assessment and Management of Hyponatremia

Initial Assessment: Determine Acuity and Severity

Begin by assessing symptom severity and onset timing, as these factors dictate the urgency and aggressiveness of treatment. 1

Symptom Classification

• Severe symptoms (medical emergency): confusion, delirium, altered consciousness, seizures, coma, or respiratory distress—these require immediate hypertonic saline regardless of sodium level 1, 2
• Moderate symptoms: nausea, vomiting, headache, muscle cramps, gait instability, lethargy, or weakness 2
• Mild/asymptomatic: may have subtle cognitive impairment or increased fall risk, but no overt neurological symptoms 2, 3

Timing Classification

• Acute hyponatremia (<48 hours): causes more severe symptoms at the same sodium level and can be corrected more rapidly without risk of osmotic demyelination 1, 2
• Chronic hyponatremia (>48 hours): requires slower correction (maximum 8 mmol/L in 24 hours) to prevent osmotic demyelination syndrome 1, 4

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Diagnostic Workup

Obtain serum and urine osmolality, urine sodium, urine electrolytes, serum uric acid, and assess extracellular fluid volume status to determine the underlying cause. 1

Essential Laboratory Tests

• Serum sodium, osmolality, glucose: confirm true hyponatremia and exclude pseudohyponatremia from hyperglycemia 1, 5
• Urine osmolality and urine sodium: differentiate causes—urine osmolality >100 mOsm/kg suggests impaired water excretion; urine sodium <30 mmol/L predicts response to saline (71-100% positive predictive value) 1
• Serum uric acid: <4 mg/dL has 73-100% positive predictive value for SIADH 1
• Thyroid-stimulating hormone (TSH) and morning cortisol: exclude hypothyroidism and adrenal insufficiency, which can mimic SIADH 1

Volume Status Assessment

Physical examination alone is unreliable (sensitivity 41%, specificity 80%), so combine clinical findings with laboratory data. 1

• Hypovolemic signs: orthostatic hypotension, dry mucous membranes, decreased skin turgor, flat neck veins 1
• Euvolemic: no edema, normal blood pressure, moist mucous membranes 1
• Hypervolemic signs: peripheral edema, ascites, jugular venous distention, pulmonary congestion 1, 5

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Treatment Based on Symptom Severity

Severe Symptomatic Hyponatremia (Emergency)

Administer 3% hypertonic saline immediately with a target correction of 6 mmol/L over 6 hours or until severe symptoms resolve. 1

• Dosing: 100 mL boluses of 3% NaCl over 10 minutes, repeat up to three times at 10-minute intervals 1
• Monitoring: check serum sodium every 2 hours during initial correction 1
• Maximum correction: never exceed 8 mmol/L in any 24-hour period to prevent osmotic demyelination syndrome 1, 4
• ICU admission: required for close monitoring during active correction 1

Asymptomatic or Mildly Symptomatic Hyponatremia

Treatment is based on volume status and underlying cause, with slower correction rates. 1

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Treatment Based on Volume Status

Hypovolemic Hyponatremia

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

• Initial infusion rate: 15-20 mL/kg/h, then 4-14 mL/kg/h based on response 1
• Urine sodium <30 mmol/L predicts good response to saline infusion 1
• For severe dehydration with neurological symptoms: consider hypertonic saline with careful monitoring 1

Euvolemic Hyponatremia (SIADH)

Fluid restriction to 1 L/day is the cornerstone of treatment for mild to moderate cases. 1

• If no response to fluid restriction: add oral sodium chloride 100 mEq three times daily 1
• For severe symptoms or sodium <120 mEq/L: administer 3% hypertonic saline 1
• Pharmacological options for resistant cases: vasopressin receptor antagonists (tolvaptan 15 mg once daily, titrate to 30-60 mg), demeclocycline, or lithium 1, 3

In neurosurgical patients, distinguish SIADH from cerebral salt wasting (CSW)—CSW requires volume and sodium replacement, NOT fluid restriction. 1

Hypervolemic Hyponatremia (Heart Failure, Cirrhosis)

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

• 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 may worsen edema and ascites 1
• Vasopressin receptor antagonists (tolvaptan) may be considered for persistent severe hyponatremia despite fluid restriction and maximization of guideline-directed medical therapy 1

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Medication-Induced Hyponatremia

Review all medications, particularly diuretics, SSRIs, carbamazepine, NSAIDs, opioids, and chemotherapy agents (platinum-based, vinca alkaloids). 1

• Discontinue offending medications when possible 1
• Thiazide diuretics are a common cause—stop if sodium <125 mmol/L 1
• For patients on diuretics with sodium 126-135 mmol/L: continue diuretics but monitor electrolytes closely; water restriction is not recommended at this level 1

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Critical Correction Rate Guidelines

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

Standard-Risk Patients

• Target correction rate: 4-8 mmol/L per day, not exceeding 10-12 mmol/L in 24 hours 1

High-Risk Patients (Advanced Liver Disease, Alcoholism, Malnutrition, Prior Encephalopathy)

• Target correction rate: 4-6 mmol/L per day, with an absolute maximum of 8 mmol/L in 24 hours 1
• Risk of osmotic demyelination syndrome: 0.5-1.5% even with careful correction 1

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 in serum sodium 1
• Target: bring the total 24-hour correction back to ≤8 mmol/L from baseline 1

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Special Populations and Pitfalls

Cirrhotic Patients

• Hyponatremia in cirrhosis reflects worsening hemodynamic status and increases risk of hepatic encephalopathy (OR 2.36), hepatorenal syndrome (OR 3.45), and spontaneous bacterial peritonitis (OR 3.40) 1
• Even mild hyponatremia (130-135 mmol/L) should not be ignored in cirrhotic patients 1, 2
• Tolvaptan use in cirrhosis carries higher risk of gastrointestinal bleeding (10% vs 2% placebo) and should be used with extreme caution 1

Neurosurgical Patients

Cerebral salt wasting (CSW) is more common than SIADH in neurosurgical patients and requires fundamentally different treatment. 1

• CSW treatment: volume and sodium replacement with isotonic or hypertonic saline, fludrocortisone 0.1-0.2 mg daily for severe symptoms 1
• Never use fluid restriction in CSW—it worsens outcomes and can precipitate cerebral ischemia 1
• In subarachnoid hemorrhage patients at risk of vasospasm: avoid fluid restriction; consider fludrocortisone or hydrocortisone to prevent natriuresis 1

Common Pitfalls to Avoid

• Overly rapid correction (>8 mmol/L in 24 hours) leading to osmotic demyelination syndrome 1
• Inadequate monitoring during active correction 1
• Using fluid restriction in CSW instead of volume replacement 1
• Failing to recognize and treat the underlying cause 1
• Using hypertonic saline in hypervolemic hyponatremia without life-threatening symptoms 1
• Ignoring mild hyponatremia (130-135 mmol/L) as clinically insignificant—it increases fall risk (21% vs 5%) and mortality (60-fold increase with sodium <130 mmol/L) 1, 2

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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