How do you classify hyponatremia in a patient?

Classification of Hyponatremia

Hyponatremia is classified based on three key parameters: severity (by serum sodium level), volume status (hypovolemic, euvolemic, or hypervolemic), and acuity (acute vs. chronic), with this systematic approach guiding both diagnosis and treatment. 1, 2, 3

Classification by Severity

Hyponatremia severity is determined by absolute serum sodium concentration:

• Mild hyponatremia: Serum sodium 130-134 mmol/L (or 126-135 mmol/L by some definitions) 1, 3
• Moderate hyponatremia: Serum sodium 120-129 mmol/L (or 120-125 mmol/L) 1, 3
• Severe hyponatremia: Serum sodium <120 mmol/L 1, 3

The classical definition uses <135 mmol/L as the threshold, though clinically significant hyponatremia typically begins at <131 mmol/L, where evaluation and treatment should be initiated. 4, 1

A critical pitfall is ignoring mild hyponatremia (130-135 mmol/L) as clinically insignificant—even at these levels, patients face increased fall risk (21% vs. 5% in normonatremic patients) and 60-fold increased mortality when sodium drops below 130 mmol/L. 1

Classification by Volume Status

Volume status assessment is the cornerstone of hyponatremia classification, though physical examination alone has poor accuracy (sensitivity 41.1%, specificity 80%). 1, 5 This classification determines the underlying pathophysiology and treatment approach:

Hypovolemic Hyponatremia

• Clinical features: Orthostatic hypotension, dry mucous membranes, decreased skin turgor, flat neck veins 1, 5
• Pathophysiology: True sodium and volume depletion 1, 6
• Urine sodium interpretation:
  • <30 mmol/L suggests extrarenal losses (GI losses, burns, third-spacing) with 71-100% positive predictive value for saline responsiveness 1, 5

  • 20 mmol/L suggests renal losses (diuretics, cerebral salt wasting, adrenal insufficiency, salt-losing nephropathy) 1, 5

Euvolemic Hyponatremia

• Clinical features: No edema, no orthostatic hypotension, normal skin turgor, moist mucous membranes 1
• Pathophysiology: Water retention without proportional sodium retention, most commonly from SIADH 1, 7, 6
• Diagnostic criteria for SIADH: Hypotonic hyponatremia with urine osmolality >300-500 mOsm/kg, urine sodium >20-40 mmol/L, normal renal/adrenal/thyroid function, and euvolemic state 1, 5, 7
• Serum uric acid <4 mg/dL has 73-100% positive predictive value for SIADH 1, 5

Hypervolemic Hyponatremia

• Clinical features: Peripheral edema, ascites, jugular venous distention, pulmonary congestion 1, 6
• Pathophysiology: Total body sodium and water excess with proportionally greater water excess 1, 6
• Common causes: Heart failure, cirrhosis, nephrotic syndrome, advanced renal failure 1, 6
• Key point: In cirrhosis, approximately 60% of patients develop hypervolemic hyponatremia due to non-osmotic vasopressin hypersecretion and impaired free water clearance 1

Classification by Acuity

Timing of hyponatremia development critically determines correction rates and risk of complications:

• Acute hyponatremia: Onset <48 hours, can be corrected more rapidly without risk of osmotic demyelination syndrome 1
• Chronic hyponatremia: Onset >48 hours, requires cautious correction with maximum 8 mmol/L increase in 24 hours to prevent osmotic demyelination syndrome 4, 1, 2, 3

The distinction between acute and chronic is crucial because overly rapid correction of chronic hyponatremia (>8 mmol/L in 24 hours) causes osmotic demyelination syndrome, while acute hyponatremia can be corrected rapidly without this risk. 1, 2

Classification by Symptom Severity

Symptom-based classification guides urgency and aggressiveness of treatment:

• Asymptomatic or mild symptoms: Nausea, vomiting, weakness, headache, mild neurocognitive deficits 2, 3
• Moderate symptoms: Confusion, disorientation, gait disturbances 2
• Severe symptoms (medical emergency): Seizures, coma, altered mental status, cardiorespiratory distress requiring immediate 3% hypertonic saline 1, 2, 3

Symptom severity depends on both the absolute sodium level and the rapidity of decline—a patient with acute drop to 125 mmol/L may have severe symptoms while a patient with chronic 120 mmol/L may be asymptomatic. 2

Special Classification Considerations in Neurosurgical Patients

In neurosurgical patients, distinguishing between SIADH and cerebral salt wasting (CSW) is critical because they require opposite treatments:

• SIADH: Euvolemic state, CVP 6-10 cm H₂O, treated with fluid restriction 4, 1, 5
• CSW: Hypovolemic state, CVP <6 cm H₂O, evidence of volume depletion, treated with volume and sodium replacement (never fluid restriction) 4, 1, 5

Using fluid restriction in CSW worsens outcomes and increases risk of cerebral ischemia, particularly in subarachnoid hemorrhage patients at risk for vasospasm. 4, 1

Diagnostic Algorithm for Classification

1. Confirm true hyponatremia: Check serum osmolality to exclude pseudohyponatremia (hyperglycemia, hyperlipidemia) 1, 5, 6
2. Assess volume status: Physical examination supplemented by urine sodium, CVP if available 1, 5
3. Measure urine osmolality and sodium:
   • Urine osmolality <100 mOsm/kg suggests appropriate ADH suppression (primary polydipsia) 1
   • Urine osmolality >100 mOsm/kg with urine sodium >20-40 mmol/L suggests SIADH in euvolemic patients 1, 5
4. Determine acuity: History of onset timing (<48 hours vs. >48 hours) 1
5. Assess symptom severity: Neurological examination for signs requiring emergent treatment 1, 2, 3

A common pitfall is obtaining ADH and natriuretic peptide levels—these are not supported by evidence and should not delay treatment. 1, 5