What causes hyponatremia, particularly in geriatric individuals or those with a history of dementia?

What Causes Hyponatremia

Hyponatremia results from an imbalance between water and sodium, most commonly due to excess water retention relative to sodium rather than absolute sodium depletion. 1

Primary Mechanisms

Dilutional Hyponatremia (Most Common)

• Excess water retention is the predominant mechanism, occurring when antidiuretic hormone (ADH/vasopressin) activity increases inappropriately, leading to free water reabsorption in the renal collecting ducts 2
• This dilutes plasma sodium concentrations while increasing blood volume 2

Depletional Hyponatremia (Less Common)

• Represents an absolute deficiency of sodium with a relative excess of body water compared to sodium concentration 2
• Typically occurs in hypovolemic states 2

Causes by Volume Status

Hypovolemic Hyponatremia

Extrarenal losses (urine sodium <30 mmol/L):

• Gastrointestinal fluid losses (vomiting, diarrhea) 3, 4
• Severe burns 5
• Excessive sweating 6

Renal losses (urine sodium >20 mmol/L):

• Diuretic use, particularly thiazides 5, 6
• Cerebral salt wasting in neurosurgical patients 3, 7
• Adrenal insufficiency 5
• Salt-losing nephropathy 7

Euvolemic Hyponatremia

Syndrome of Inappropriate Antidiuresis (SIADH) is the primary cause:

• Malignancies (especially small cell lung cancer) 3, 7
• CNS disorders (meningitis, encephalitis, stroke, subarachnoid hemorrhage) 3, 7
• Pulmonary diseases (pneumonia, tuberculosis) 7
• Medications: SSRIs, carbamazepine, NSAIDs, opioids, chemotherapy agents (platinum-based, vinca alkaloids) 3
• Postoperative states 3
• Pain, nausea, and stress (nonosmotic stimuli for AVP release) 3

Other euvolemic causes:

• Hypothyroidism 5, 3
• Adrenal insufficiency 3
• Excessive free water intake during exercise 6
• Very low-salt diets 6
• Beer potomania (excessive alcohol consumption with poor nutrition) 3, 6

Hypervolemic Hyponatremia

Edematous states with impaired water excretion:

• Congestive heart failure: Low cardiac output triggers compensatory neurohormonal activation, increasing AVP activity and causing water retention 2
• Liver cirrhosis with ascites: Portal hypertension causes systemic vasodilation, decreased effective plasma volume, and activation of renin-angiotensin-aldosterone system, leading to excessive sodium and water reabsorption 3
• Nephrotic syndrome 5
• Advanced renal failure 7

Special Populations

Geriatric Patients

• Impaired thirst mechanism increases risk 4
• Cognitive impairment is both a risk factor for and consequence of hyponatremia 5
• History of severe hypoglycemia in older adults with type 2 diabetes is associated with greater risk of dementia, and conversely, cognitive impairment increases risk of subsequent severe hypoglycemia 5
• Even mild hyponatremia (130-135 mmol/L) is associated with increased fall risk (21% vs 5% in normonatremic patients) and fractures 3, 1

Patients with Dementia

• Cognitive impairment at baseline or declining cognitive function significantly increases risk of severe hyponatremia 5
• Hyponatremia itself worsens cognitive function, creating a bidirectional relationship 1

Hospitalized Patients

• Hospital-acquired hyponatremia from hypotonic IV fluids in the setting of elevated AVP affects 15-30% of hospitalized patients and is entirely preventable by using isotonic maintenance fluids 3
• Acute illness states (pancreatitis, postoperative) trigger nonosmotic AVP release through pain, nausea, and stress 3

Medication-Induced Hyponatremia

High-risk medications requiring close monitoring 5:

• Desmopressin (perioperatively for Von Willebrand disease) 5
• Antiepileptic medications (carbamazepine) 5, 3
• Chemotherapeutic agents (IV cyclophosphamide, vincristine) 5
• Antidepressants including trazodone 3

Common Pitfalls

• Ignoring mild hyponatremia (130-135 mmol/L) as clinically insignificant, when it actually increases mortality 60-fold (11.2% vs 0.19%) and significantly increases fall risk 3
• Failing to assess volume status accurately, as physical examination alone has poor sensitivity (41.1%) and specificity (80%) 3
• Not distinguishing SIADH from cerebral salt wasting in neurosurgical patients, as they require opposite treatments (fluid restriction vs. volume replacement) 3, 7
• Overlooking medication causes, particularly in elderly patients on multiple medications 3