What condition is consistent with hyponatremia and hypoosmolality in a critically ill patient?

Hypoosmolar Hyponatremia (SIADH)

A serum sodium of 130 mEq/L with plasma osmolality of 260 mOsm/kg is most consistent with the syndrome of inappropriate antidiuretic hormone secretion (SIADH), which is the most common cause of euvolemic hypoosmolar hyponatremia in critically ill patients. 1

Diagnostic Confirmation

The combination of these laboratory values establishes hypoosmolar hyponatremia:

• Plasma osmolality of 260 mOsm/kg is significantly below the normal range of 275-290 mOsm/kg, confirming true hypoosmolarity rather than pseudohyponatremia 1, 2
• Serum sodium of 130 mEq/L represents moderate hyponatremia (mild is 130-134 mEq/L, moderate is 120-129 mEq/L) 3, 4
• This pattern excludes hypertonic hyponatremia (from hyperglycemia) and isotonic hyponatremia (pseudohyponatremia from hyperlipidemia or hyperproteinemia) 5, 2

SIADH as the Primary Diagnosis

SIADH is characterized by inappropriately concentrated urine despite low plasma osmolality in a euvolemic patient, and is the most common paraneoplastic endocrine phenomenon, particularly with small cell lung cancer occurring in 10-45% of cases 1. The diagnostic criteria include:

• Hypotonic hyponatremia with plasma osmolality <275 mOsm/kg 1
• Inappropriately elevated urine osmolality (typically >300 mOsm/kg when it should be maximally dilute at <100 mOsm/kg) 1, 5
• Urine sodium concentration >20-40 mEq/L despite low serum sodium 6, 5
• Clinical euvolemia (no edema, no orthostatic hypotension, normal skin turgor) 6, 1
• Normal thyroid, adrenal, and renal function 1, 7

Differential Diagnosis by Volume Status

The volume status assessment is critical for distinguishing SIADH from other causes:

• Euvolemic hyponatremia (SIADH): No signs of volume depletion or overload, urine sodium >20-40 mEq/L, urine osmolality >300 mOsm/kg 6, 5
• Hypovolemic hyponatremia: Orthostatic hypotension, dry mucous membranes, decreased skin turgor, urine sodium typically <30 mEq/L if extrarenal losses 6, 5
• Hypervolemic hyponatremia: Peripheral edema, ascites, jugular venous distention from heart failure or cirrhosis 6, 5

Common Causes in Critically Ill Patients

SIADH in the critical care setting is most commonly caused by:

• Malignancies, particularly small cell lung cancer (10-45% incidence), but also head and neck cancers 1, 7
• CNS disorders including subarachnoid hemorrhage, meningitis, encephalitis, and head trauma 6, 3
• Pulmonary diseases such as pneumonia, tuberculosis, and acute respiratory failure 1, 3
• Medications including SSRIs, carbamazepine, cyclophosphamide, platinum-based chemotherapy, vinca alkaloids, and opioids 6, 1
• Postoperative states and pain, nausea, stress as nonosmotic stimuli for ADH release 6, 7

Critical Pitfalls to Avoid

• Failing to distinguish SIADH from cerebral salt wasting (CSW) in neurosurgical patients, as they require opposite treatments—SIADH needs fluid restriction while CSW requires volume and sodium replacement 6, 1
• Administering normal saline to euvolemic SIADH patients, which can paradoxically worsen hyponatremia since the kidneys will excrete the sodium while retaining the free water 6
• Overly rapid correction exceeding 8 mmol/L in 24 hours, which risks osmotic demyelination syndrome, a devastating and potentially fatal complication 6, 4
• Ignoring mild hyponatremia (130-135 mEq/L) as clinically insignificant, when even mild chronic hyponatremia increases fall risk (23.8% vs 16.4%), fracture rates, and mortality 6, 4