Concerted action of the hypothalamic-pituitary axis to influence water intake through thirst and water excretion via the effect of vasopressin, on renal collecting duct water permeability, is the prime mechanism for the regulation of overall body fluid concentration.

Sodium being the principal extracellular cation experiences major disturbances during any abnormalities in overall effective body fluid concentration. hyponatremia in its severe and chronic stage may lead to significant symptoms, primarily related to central nervous system function. Persistent hyponatremia or its rapid correction can lead to permanent neurologic damage. Thus chronic hyponatremia demands extra precautions. 

Hypernatremia can also cause central nervous system dysfunction. An article discusses the normal regulation of tonicity and serum sodium concentration and the diagnosis and management of hypo- and hypernatremia.

Treatment of Hyponatremia 

Treatment of Hypertonic Hyponatremia 

Translocational hyponatremia secondary to hyperglycemia improves with lowering of blood glucose level. Aggressive volume repletion with isotonic fluid can also be required to correct volume depletion from the glucosuria-driven osmotic diuresis and account for intracellular translocation of water with glucose in response to insulin. 

Complications of Treatment of Hypotonic Hyponatremia 

Brain cell may dehydrate and shrink if their surrounding tonicity increases faster than it can reaccumulate effective osmoles. Rapid correction of hyponatremia can lead to Osmotic demyelination syndrome (ODS), sequelae of which are often irreversible and include dysphagia, dysarthria, spasticity, behavioural disturbance, cognitive impairment, delirium, seizures, quadriparesis, coma, and “locked-in” syndrome. Neurologic deterioration in ODS shows up several days after an initial treatment-induced improvement in the neurologic symptoms from the hyponatremia. 

Acute hypotonic hyponatremia of less than 24 to 48 hours history lacks complete brain adaptation and thus do not possess a risk of ODS. Patients with an initial [Na+ ] > 125 mEq/L are also unlikely to encounter ODS.

Risk factors for ODS include patients with chronic hypotonic hyponatremia with a presenting [Na+ ] < 105 mEq/L, alcoholism, advanced liver disease, malnutrition and hypokalemia.

Treatment of Hypotonic Hyponatremia 

Worsening of hyponatremia can be stopped with Electrolyte-free water restriction and discontinuation of thiazide diuretic treatment. In cases of maximally diluted urine, restricting fluid ingestion in primary polydipsia or increasing solute intake and thus the potential for electrolyte-free water excretion in a patient following an otherwise solute-deficient diet gives optimum result. 

Patients with severe hyponatremia due to primary polydipsia can have rapid correction of [Na+ ] with fluid restriction. Close monitoring and measures to replace or retard water loss is essential.

Source: Seay NW, Lehrich RW, Greenberg A. Diagnosis and Management of Disorders of Body Tonicity—Hyponatremia and Hypernatremia: Core Curriculum 2020. Am J Kidney Dis. 75(2): 272-286.