Hyponatremia is a pathophysiological condition defined by serum sodium levels of less than 135 mmol/L. It is unrelated to the total sodium content in the body and can occur in various contexts, including sodium deficiency, water retention, or concurrent retention of both sodium and water. Serum sodium levels reflect the effective extracellular osmolality and influence intracellular fluid volume. Hyponatremia is therefore indicative of hypotonicity and is also referred to as hyponatremic hypotonic syndrome.
Classification
Sodium-Deficient Hyponatremia (Hypotonic Dehydration)
This condition involves a reduction in both total body sodium and intracellular sodium, resulting in decreased serum sodium concentration. It is seen in cases such as gastrointestinal fluid losses, loss of water and sodium via the skin, losses associated with fluid migration into body cavities, renal sodium loss, and ascitic drainage.
Dilutional Hyponatremia
This form of hyponatremia arises from water overload, which dilutes sodium in the blood. Total sodium levels may be normal or increased, but intracellular fluid and serum sodium concentrations are reduced. Cases include psychogenic polydipsia, syndrome of inappropriate antidiuretic hormone secretion (SIADH), stress responses, and ascites in liver cirrhosis.
Redistributive Hyponatremia
This rare form occurs when sodium shifts from the extracellular to the intracellular compartment in the context of sodium deficiency. Total body sodium remains normal, while intracellular sodium increases, leading to reduced serum sodium levels.
Idiopathic Hyponatremia
This condition occurs due to intracellular osmotic pressure reduction caused by protein catabolism within the cell. As a result, water moves from the intracellular to the extracellular compartment. It is commonly seen in malignant tumors, end-stage liver cirrhosis, malnutrition, advanced age or frailty, and the terminal stages of other chronic illnesses. It is also referred to as consumptive hyponatremia.
Cerebral Salt Wasting Syndrome (CSWS)
This condition results from hypothalamic or brainstem injury, which disrupts the neural connection between the hypothalamus and the kidneys. It leads to osmotic diuresis in the distal tubules and reductions in serum sodium, chloride, and potassium levels, with corresponding increases in urinary excretion of these electrolytes.
In any patient with neurological damage presenting with hyponatremia, it is crucial to differentiate between CSWS and SIADH. CSWS is associated with reduced blood volume, dehydration symptoms, lowered plasma osmolality, and significantly increased urinary sodium and chloride. Conversely, SIADH is characterized by increased blood volume, decreased plasma osmolality, and reduced central venous pressure. Volume depletion is a key diagnostic point differentiating CSWS, and elevated AVP (arginine vasopressin) levels can help evaluate the extent of blood volume reduction.
Diagnosis and Differential Diagnosis
These can be seen in the sections on hypotonic dehydration, water excess, and water intoxication for details. Pseudohyponatremia caused by hyperglycemia is one of the most common differential diagnoses. Other contributing factors include severe dyslipidemia and hyperproteinemia. In cases of hyponatremia attributed to hyperglycemia, corrected serum sodium levels can be calculated as follows:
Corrected Sodium Concentration = Measured Serum Sodium + 2.4 × (Blood Glucose - 5.5)/5.5
Treatment
Management involves actively treating the underlying disease and correcting electrolyte imbalances.
For CSWS caused by intracranial conditions, supplementation with both electrolytes and water is necessary. In some cases, AVP antagonists such as tolvaptan, conivaptan, or mozavaptan may be used. Additionally, fludrocortisone (0.05–0.1 mg per dose, twice daily) may be considered, although long-term use is not recommended.