Is the hyponatraemia in a 78‑year‑old woman with urine sodium 95 mmol/L, urine osmolality 418 mOsm/kg, blood urea nitrogen/creatinine ratio 33:1, low serum creatinine, estimated glomerular filtration rate 121 mL/min/1.73 m², and extensive vitamin supplementation due to SIADH rather than hypovolaemia, and what is the appropriate management?

Diagnosis: SIADH with Improving Hyponatremia

This 78-year-old woman has SIADH, not hypovolemia, based on her high urine sodium (95 mmol/L), concentrated urine (osmolality 418 mOsm/kg), and clinical euvolemia despite recent improvement in serum sodium from 127 to 134 mmol/L with fluid restriction. 1

Diagnostic Reasoning

The laboratory findings definitively point to SIADH:

• Urine sodium >20–40 mmol/L (hers is 95 mmol/L) with urine osmolality >300 mOsm/kg (hers is 418 mOsm/kg) in the setting of hyponatremia confirms inappropriate urinary concentration, the hallmark of SIADH. 1, 2

• The elevated BUN/creatinine ratio (33:1) with low serum creatinine (0.5 mg/dL) and supranormal eGFR (121 mL/min/1.73 m²) reflects volume expansion from water retention, not dehydration. In true hypovolemia, you would expect elevated creatinine with prerenal azotemia, not a low creatinine with high eGFR. 1

• Her clinical response to fluid restriction—sodium rising from 127 to 134 mmol/L—confirms the diagnosis of SIADH, as fluid restriction is the cornerstone therapy for this condition. 1, 2

Why this is NOT hypovolemia:

• Hypovolemic hyponatremia typically presents with urine sodium <30 mmol/L (positive predictive value 71–100% for saline responsiveness), not 95 mmol/L. 1

• True volume depletion would manifest with orthostatic hypotension, dry mucous membranes, decreased skin turgor, and elevated creatinine—none of which are described here. 1

• The supranormal eGFR (121 mL/min/1.73 m²) is inconsistent with hypovolemia, which causes prerenal azotemia and reduced GFR. 1

Management Strategy

Continue fluid restriction to 1 L/day as first-line therapy, as this has already proven effective in raising her sodium from 127 to 134 mmol/L. 1, 2

Monitoring Protocol

• Check serum sodium every 24–48 hours initially to ensure stable correction, then weekly once stable. 1

• Target a correction rate of 4–6 mmol/L per day, never exceeding 8 mmol/L in 24 hours, as this patient is at high risk for osmotic demyelination syndrome given her age and potential for malnutrition. 1

If Fluid Restriction Fails

If sodium drops below 125 mmol/L or symptoms develop despite fluid restriction, add oral sodium chloride 100 mEq (approximately 6 grams) three times daily. 1, 2

For persistent hyponatremia refractory to fluid restriction and salt supplementation, consider tolvaptan 15 mg once daily, titrating to 30–60 mg as needed. 1, 3 However, tolvaptan requires intensive monitoring (serum sodium every 2 hours for the first 8 hours after initiation) and carries risks including thirst, polyuria, and potential drug interactions with her vitamin supplements if any contain CYP3A inhibitors. 3

Address Underlying Causes

Review all medications and vitamin supplements for potential SIADH triggers, including SSRIs, carbamazepine, NSAIDs, opioids, and certain chemotherapy agents. 1

Evaluate for common causes of SIADH in elderly patients: malignancy (especially lung cancer), CNS disorders, pulmonary disease, and medications. 1, 2

Critical Safety Considerations

Never use hypertonic saline in this asymptomatic patient with chronic hyponatremia, as rapid correction risks osmotic demyelination syndrome. 1 Hypertonic saline is reserved only for severe symptomatic hyponatremia with seizures, coma, or altered mental status. 1, 2

Do not administer normal saline, as this will worsen hyponatremia in SIADH by providing free water that will be retained. 1 Normal saline is appropriate only for hypovolemic hyponatremia with urine sodium <30 mmol/L. 1

Avoid exceeding 8 mmol/L correction in any 24-hour period—her current sodium of 134 mmol/L is acceptable, and aggressive correction toward "normal" is unnecessary and dangerous. 1

Common Pitfalls to Avoid

• Misinterpreting the elevated BUN/creatinine ratio as dehydration when it actually reflects volume expansion from SIADH. 1

• Administering normal saline based on the elevated BUN/creatinine ratio, which would worsen hyponatremia in SIADH. 1

• Ignoring the extensive vitamin supplementation as a potential contributor to SIADH or drug interactions. 1

• Failing to monitor for osmotic demyelination syndrome signs (dysarthria, dysphagia, oculomotor dysfunction, quadriparesis) if correction becomes too rapid. 1