Etiopathogenesis, diagnostics and
therapy of
hyponatremias are summarized for clinicians.
Hyponatremia is the most common
electrolyte abnormality. Mild to moderate
hyponatremia and severe
hyponatremia are found in 15-30% and 1-4% of hospitalized patients, respectively. Pathophysiologically,
hyponatremias are classified into two groups:
hyponatremia due to non-osmotic hypersecretion of
vasopressin (
hypovolemic, hypervolemic, euvolemic) and
hyponatremia of non-hypervasopressinemic origin (pseudohyponatremia,
water intoxication, cerebral
salt wasting syndrome). Patients with mild
hyponatremia are almost always asymptomatic. Severe
hyponatremia is usually associated with central nervous system symptoms and can be life-threatening. Diagnostic evaluation of patients with
hyponatremia is directed toward identifying the extracellular fluid volume status, the neurological symptoms and signs, the severity and duration of
hyponatremia, the rate at which
hyponatremia developed. The first step to determine the probable cause of
hyponatremia is the differentiation of the hypervasopressinemic and non-hypervasopressinemic
hyponatremias with measurement of plasma osmolality,
glucose,
lipids and
proteins. For further differential diagnosis of
hyponatremia, the determination of urine osmolality, the clinical assessment of extracellular fluid volume status and the measurement of urine
sodium concentration provide important information. The most important representative of euvolemic
hyponatremias is
SIADH. The diagnosis of
SIADH is based on the exclusion of other hyponatremic conditions; low plasma osmolality (<275 mosmol/kg) and inappropriate urine concentration (urine osmolality >100 mosmol/kg) are of pathognomic value. Acute (<48 hrs) severe
hyponatremia (<120 mmol/l) necessitates emergency care with rapid restoration of normal osmotic milieu (1 mmol/l/hr increase rate of serum
sodium). Patients with chronic symptomatic
hyponatremia have a high risk of osmotic
demyelination syndrome in brain if rapid correction of the plasma
sodium occurs (maximal rate of correction of serum
sodium should be 0.5 mmol/l/hr or less). The conventional treatments for chronic asymptomatic
hyponatremia (except
hypovolemic patients) include water restriction and/or the use of
demeclocycline or
lithium or
furosemide and
salt supplementation.
Vasopressin receptor antagonists have opened a new forthcoming therapeutic era.
V2 receptor antagonists, such as
lixivaptan,
tolvaptan,
satavaptan and the V2+V1A receptor antagonist
conivaptan promote the
electrolyte-sparing excretion of free water and lead to increased serum
sodium.