Hydroelectrolytic syndromes in neuroanesthesia and neurocritical care

Table 1 Hyponatremia syndromes and laboratory workup

Etiology	Volume status	Serum osmolality (mOsm/kg)	Urine osmolality	Urine Na+	Other features
SIADH	Euvolemic	↓ (< 280)	↑ (> 100 mOsm/kg, often > serum)	↑ (> 40 mEq/L)	↓ Serum uric acid; high FeUA before correction (> 11%) that normalizes after correction (4%-11%)
Cerebral salt wasting	Hypovolemic	↓ (< 280)	↑ (> 100, less concentrated than SIADH)	↑ (> 40 mEq/L)	↑ natriuretic peptides; persistent high FeUA (> 11%) even after Na+ correction
Diuretic-induced	Hypovolemic	↓ (< 280)	Variable (often ↑)	Variable (> 20 mEq/L)	History of loop or thiazide use; UNa interpretation may be confounded by recent diuretics
Excess hypotonic fluids	Euvolemic or hypervolemic	↓ (< 280)	↓ (< 100 mOsm/kg)	↓ (< 30 mEq/L)	Large-volume hypotonic IV fluids or low-solute intake (e.g., beer potomania)
Adrenal insufficiency	Euvolemic	↓ (< 280)	↑ (> 100 mOsm/kg)	↑ (> 40 mEq/L)	↓ Cortisol; hyponatremia resistant until glucocorticoid replaced

Confirm true hypotonic hyponatremia with serum osmolality < 280 mOsm/kg and rule out pseudohyponatremia. Volume status (clinical exam, hemodynamics) plus urine indices (osmolality, Na⁺) are essential to distinguish syndrome of inappropriate antidiuretic hormone secretion (euvolemic, concentrated urine, high urine Na) from cerebral salt wasting syndrome (hypovolemic, similar labs but with hypovolemia signs). Iatrogenic contributors (diuretics, hypotonic fluids) and endocrine causes (adrenal insufficiency) must always be considered. Continuous monitoring and tailored therapy (fluid restriction or vaptans for syndrome of inappropriate antidiuretic hormone secretion vs volume/sodium repletion for cerebral salt wasting syndrome) are critical. FeUA: Fractional excretion of uric acid; IV: Intravenous; SIADH: Syndrome of inappropriate antidiuretic hormone secretion; UNa: Urine Na.